Skip to Main Content
Text size: SmallMediumLargeExtra-Large

Chapter 8: Personal and Provider Approaches to Oral Health

 Home  |  Contents  |  Links  |  Search Tips  |  Executive Summary  |  Part One
Part Two  |  Part Three  |  Part Four  |  Part Five  

Oral health is not a given. It takes conscious and repeated efforts on the part of the individual, caregivers, health care providers, and the community. For the individual, daily hygiene routines and healthy lifestyle behaviors provide a frontline defense in disease prevention and health promotion. Equally important are periodic professional assessments of the individual's oral health status, which may include diagnostic, preventive, and therapeutic services and counseling. Community activities complement personal and provider approaches to oral health. As discussed in the previous chapter, these include water fluoridation, dental sealant applications for children, tobacco cessation campaigns, the use of mouthguards in sports, and a variety of other school- and community-based oral health promotion and disease prevention activities. The interaction of these components is critical to oral health, as it is to overall health. In particular, there is now a better understanding of the relationship of individual health to the health of the community in which the individual lives, and the importance of this relationship is one of the underlying premises of Healthy People 2010. This chapter discusses actions individuals can take to maintain their oral health and prevent disease, and reviews emerging approaches taken by dentists and other health care providers to promote oral health, assess risks, and prevent disease.

back to top


Sound personal hygiene practices and adherence to a healthy lifestyle are the mainstays of personal approaches to oral health. Long before the germ theory of disease, the need for tooth cleaning was recognized—if only to rid the mouth of food debris, eliminate odor, and improve appearance. Tools developed for this purpose have ranged from primitive tooth sticks and picks, still used in parts of the world, to the water irrigators and electronic toothbrushes available in industrialized societies. An impressive array of oral care products greets the shopper in supermarkets and pharmacies today. Beyond the dozens of toothbrush shapes and sizes, there are flavored and textured dental flosses, floss holders, rubber tips, toothpicks, small brushes for cleaning between teeth, scores of dentifrices, and a range of fluoride-containing, antitartar, and antiseptic mouthrinses.

Daily oral hygiene efforts contribute to the prevention of dental caries and periodontal diseases. The biofilm on tooth and root surfaces (dental plaque) can be disrupted to a large extent by the mechanical action of brushing and flossing. Daily efforts are necessary, not only because of food intake, but also because dental plaque is never completely removed. It starts to build up even after the most assiduous cleaning (or prophylaxis) in the dental office and even after the application of a potent antimicrobial mouthrinse. The oral and dental tissues and structures thus require more intensive daily care than do other body areas exposed to the environment.

back to top

Daily Hygiene and Dental Caries Prevention

The use of a fluoride-containing dentifrice is critical for dental caries prevention. Even more beneficial than the physical removal of plaque in toothbrushing is the delivery of a small amount of fluoride to the tooth surfaces. Investigators have conducted numerous clinical trials on fluoride dentifrices using rigorous designs and including randomized groups, double-blind designs, and placebo controls. All together, these studies provide strong evidence that using a fluoride dentifrice is effective (Clarkson et al. 1993, Lewis and Ismail 1995, Stookey et al. 1993). Fluoride dentifrices account for more than 90 percent of the market in the United States, Canada, and other developed countries (Levy 1994).

A fluoride dentifrice is an effective means of reducing the prevalence of dental caries for all persons. Although children's teeth should be cleaned daily from the time they erupt, parents and caregivers should consult a dentist or other health care provider about the use of a fluoride dentifrice for children under the age of 2. For children under 6, fluoride dentifrices should be used in small amounts to minimize swallowing of the product. Mild enamel fluorosis can result from excessive dentifrice use, because children under 6 do not have adequate control of the swallowing reflex or may intentionally swallow a flavored dentifrice. Experts recommend that for children under 6, the parent or caregiver should supervise toothbrushing, apply a pea-sized amount (0.25 gram) of dentifrice to the toothbrush, and encourage the child to spit out the excess (Bawden 1992).

Because the topical benefits of fluoride have been shown to be highly effective, and daily exposure to small amounts of fluoride can reduce the risk of dental caries in all age groups, experts recommend that all persons drink water with an optimal fluoride concentration in addition to brushing daily with a fluoride dentifrice (Bawden 1992, CDC in press). This combination provides a cost-effective and easy way to prevent dental caries and is an excellent example of the individual-community partnership. For persons at low risk of dental caries, these two exposures to fluoride may be the only ones necessary. For persons at moderate or high risk of dental caries, additional fluoride may be helpful and can come from daily use of another fluoride product. These can include mouthrinses, prescribed supplements, and professionally applied topical fluoride products (CDC in press).

back to top

Daily Hygiene and the Prevention of Periodontal Diseases

Toothbrushing and flossing also play a critical role in the prevention of periodontal diseases. Unlike dental caries prevention, prevention and control of gingivitis and periodontitis are achieved directly through the mechanical removal and disruption of dental plaque (Genco and Newman 1996). Some dentifrices also contain chemical therapeutics to control the formation of tartar (calculus) (Mandel 1995) and to reduce plaque formation and gingival inflammation (Hancock 1996). Both manual and electric toothbrushing are effective at removing plaque and preventing gingivitis (Walsh et al. 1989, Axelsson et al. 1991). Interproximal (between the teeth) cleaning is also important in maintaining gingival health (Lang et al. 1994). In one short-term evaluation of adults, the addition of flossing to the daily regimen of brushing resulted in an almost twofold reduction in gingival inflammation (Graves et al. 1989). Because preventive measures in periodontics rely mainly on the removal of bacterial plaque and calculus, methods typically include personal oral hygiene measures combined with professional diagnostic and prophylactic measures (i.e., regular exam and cleaning). Periodic professional care for removal of plaque and calculus deposits has also been demonstrated to improve the periodontal health of participants (Cutress et al. 1991, Ronis et al. 1993).

back to top

Healthy Lifestyles

There is more to the individual's role in promoting oral health and hygiene than brushing and flossing. Other behaviors that have an influence on oral health include use of tobacco and/or alcohol products, diet, oral habits such as bruxing and clenching the teeth, and use of helmets, mouthguards, or other protective devices. Table 8.1 summarizes selected behaviors that have an effect on oral, dental, and craniofacial health status. These are described more fully in Chapters 3, 7, and 10.

Individuals can obtain credible information regarding oral health from various sources, including health care providers, professional organizations, government agencies, and patient advocacy groups. Increasingly, the World Wide Web is a source for health care information. For example, the National Oral Health Information Clearinghouse offers information on oral health, with an emphasis on special care patients and their health care providers.

back to top

Care Seeking

In addition to self-care, individuals also need to seek professional health care—both dental and medical—on a regular basis and whenever a problem manifests. The recall interval is based on the provider's assessment of the individual's dental and medical history and lifestyle behaviors, among other factors. In the case of children and dependent adults, parents and caregivers are responsible for teaching and encouraging healthy behaviors and seeking timely and appropriate care. As noted at the outset, it is only through the combination of individual and professional care, reinforced by community-based health promotion and disease prevention programs, that optimal oral and general health can be achieved. The remainder of this chapter focuses on the role of the professional in oral health care.

back to top


The range of conditions and diseases that affect the craniofacial complex is extensive and can provide clinicians with important indications about the patient's general as well as oral health status. Management of the oral health–general health interface calls for interdisciplinary and coordinated care and an enhanced role for primary care providers. Dentists, oncologists, dermatologists, infectious disease specialists, hematologists, endocrinologists, plastic surgeons, and rheumatologists are just a few of the specialists who may be involved in the diagnosis and management of conditions affecting the craniofacial complex.

Dentists, their allied staff, and medical and nursing personnel are in a unique position to incorporate new approaches for prevention,1 diagnostic, and treatment strategies in their practices. Advances in oral science are providing the basis for a shift in emphasis from the repair and restoration of damaged tissues to earlier diagnoses, control of infections, and remineralization and regeneration of lost tissues. The application of risk assessment strategies and interventions tailored to individuals and groups is expanding with the increased understanding of risk factors and the development of biomarkers that signal host resistance, susceptibility, and the presence and progression of disease.

The changing demographics of the U.S. population and a greater understanding of the relationship between oral health and general health are presenting new challenges. Making clinical decisions for patients requires integrating a range of interacting biological, psychological, social, cultural, and environmental factors. In order for disease to manifest, the etiologic agent(s) must be present, the host must be susceptible, the environment conducive, and sufficient time available for the factors to interact (Figure 8.1). Early diagnosis and prompt treatment require an understanding of the pathology and of the diagnostic, prevention, and treatment modalities available. As genetic information accumulates, clinical judgments will increasingly be informed by knowledge of an individual's genetic susceptibility or resistance to particular diseases and disorders. The development of tailored treatment plans will require incorporating all these factors together with input from the patient's health providers, taking into consideration the patient's interests and needs. The following sections provide an overview of emerging approaches to clinical management and highlight selected diseases as examples.

back to top

Risk Assessment

Given the greater understanding of disease etiology, epidemiology, patient characteristics, and genetic information, it is becoming increasingly possible to determine an individual's risk of disease and tailor treatments accordingly. Risk assessment for dentistry has been defined as "the use of knowledge of factors that are associated with dental disease to determine which patients are more or less likely to prevent or control their dental disease" (Douglass 1998). The factors can include co-morbidities, medications used, and patient characteristics such as sex, age, and lifestyle behaviors, among others. By compiling such factors and sorting them by risk category, patients can be classified into high- or low-risk groups, enabling providers to make more comprehensive diagnoses and identify patients who would benefit from more aggressive prevention strategies. Such analyses conducted during the early stages of disease can result in treatments that reverse or contain the disease process (Douglass 1998). Knowledge of risk factors for oral and craniofacial diseases and disorders allows other health care providers to screen for these risk factors and contribute to improving oral health.

Risk assessment and disease prediction studies have focused primarily on dental caries and periodontal diseases (Genco 1996, Page and Beck 1997, Pitts 1998, Powell 1998). In addition, risk factors for oral and pharyngeal cancers have been explored (Johnson 1991). The evidence base for risk assessment is developing from population-based studies. It involves a research process in which a suspected risk factor is related in a multivariate model to other factors and confounders (Beck 1990). The resulting model is tested in a second group of subjects, and a targeted intervention study is conducted to confirm the predictive validity of the risk factor.

Although the application of research findings of risk assessment has begun in some practices, the prediction of future disease at the individual patient level has not yet been extensively studied. Douglass (1998) has posed six clinically oriented questions that need to be addressed if risk assessment is to be adopted into routine clinical practice:

1. Does the scientific theory or biologic logic of the risk factor fit with our current body of knowledge about the disease in question?

2. Has the technical merit of identifying the risk factor (such as imaging technologies and bacterial assays) been evaluated?

3. Has the efficacy of the risk factor in predicting disease been evaluated in terms of sensitivity, specificity, and positive and negative predictive values?2

4. Has the potential effect of the risk factor on the disease management decision been explored? Can knowledge of the presence of a particular risk factor or pattern of risk factors alter the treatment plan?

5. Has the influence of the risk factor on oral health outcomes been assessed?

6. Has the cost-effectiveness of collecting risk factor data from each patient been evaluated? Is the added expense justified either by increased effectiveness or by avoiding other expenses?

back to top

Diagnostic Tests

Whereas risk assessment aims to predict future disease and disease progression, diagnostic tests evaluate a patient's current status with regard to a specific disease or disorder. They enable the provider to formulate, in cooperation with the patient, a treatment plan. In relation to dental caries and periodontal diseases, the diagnosis ideally should not only detect the presence of disease, but also distinguish between active and arrested disease.

Today, most diagnostic tests for oral conditions are based primarily on anatomic clinical evidence. However, microbiological, pathological, immunological, genetic, and tissue metabolite tests are increasingly available and valuable. Table 8.2 cross-references diseases with categories of diagnostic tests available. The following sections describe elements of a general health assessment and highlight risk assessment, diagnosis, and prevention of selected diseases and conditions.

back to top

Oral Health Assessment

An oral health assessment involves an evaluation of an individual's overall health status, including any risk factors and personal needs that can affect health and treatment options. For the majority of craniofacial conditions, this assessment and subsequent care are coordinated with a range of health care providers, with the intent of enhancing the patient's overall health and well-being.

The information gathered for the assessment is derived from patient information, extraoral and intraoral clinical examinations, and imaging and other diagnostic tests as needed. The patient provides demographic and lifestyle behavior information and a medical and dental history, including current complaints, if any. Symptom analysis entails an additional series of questions that explore symptom onset, characteristics, and course. Figure 8.2 provide an example of a medical history form used in dental practice.

The clinician will take into consideration the patient's general appearance and ability to function, as noted by characteristics of facial symmetry or asymmetry and speech. In addition, the patient's vital signs may be assessed, and a thorough examination of the head, neck, temporomandibular joints, and other structures will be conducted. The intraoral portion of the examination involves an extensive assessment of the tissues: the lips and labial mucosa, buccal mucosa and mucobuccal fold, the floor of the mouth, tongue, hard and soft palate, oropharynx, muscles of mastication, salivary glands and saliva, gingiva, periodontium, and teeth.

Depending on the needs of the patient, the initial physical examination is usually augmented by supplementary data from radiographs and sometimes by other diagnostic tests, including tissue biopsies and samples of oral cells and fluids. Such samples can be used to type specific bacteria, viruses, or fungi or to detect elevated levels of tissue metabolites or immune system factors associated with disease. The number of such tests is increasing and will be supplemented by genetic tests to indicate an individual's susceptibility to specific diseases.

Currently, the assessment of oral and craniofacial health and disease involves intraoral radiographs as well as radiographic imaging, including arthrography, motion-based tomography, and computed tomography (Jeffcoat 1992). Intraoral radiographs permit detection of lesions between teeth and are the only widely available clinical test that can assess periodontal bone support in situ (Jeffcoat et al. 1995). Radiographs are an essential tool for treatment planning of complex prosthetic reconstructions as well as a diagnostic method to assess periodontal progression. However, the mere presence of bone loss on a radiograph does not imply progressive osseous destruction, although it does increase the patient's risk of future bone loss (Armitage 1996, Genco 2000). Radiographs have high specificity for disease progression, and low sensitivity. Because all radiographic examinations expose the patient to some, albeit small, level of ionizing radiation, current guidelines indicate that radiographs should not be taken routinely (FDA 1987), but should be prescribed after an initial assessment by the dentist.

Image processing techniques, such as digital radiography, enhance the clinician's ability to detect small intraoral osseous changes over time and aid in the detection of small changes in skeletal tissues between examinations. Direct digital radiography uses an intraoral detector to capture a radiographic image of the diagnostic area of interest (Ellwood et al. 1997, Matsuda et al. 1997). Several proposed methods for quantitative estimation of lesion mass or volumetry using digital subtraction radiography exist (Armitage 1996). A recent multicenter validation study has indicated that simulated lesions as small as 1 mg in mass may be detected with better than 90 percent sensitivity and specificity (Jeffcoat et al. 1996). These techniques are currently in use in clinical trials.

New diagnostic methods are also becoming available as adjuncts to existing methods for caries diagnosis. Comparing data between bite-wing radiographs of potential occlusal fissure lesions, Lussi et al. (1995) found that electrical resistance measurement may provide a substantial improvement in caries diagnosis.

Other imaging approaches are used to assess craniofacial anatomy, temporomandibular joints, maxillary sinuses, and other associated tissues, and in the assessment of the size and quality of bone to receive dental implants. Magnetic resonance imaging (MRI) is also receiving increased attention for craniofacial applications, such as for the assessment of the temporomandibular joints. Finally, light-based imaging of teeth and associated structures, using a small intraoral camera, gives both the patient and the provider a wide-screen view of the oral cavity, aiding in patient education.

In the course of conducting a general assessment, the clinician notes disease-specific signs and symptoms. While examining the teeth, the clinician may detect signs of relatively rare hereditary diseases such as ectodermal dyplasias, or more common destructive habits such as bruxism, where the enamel and at times the dentin may be abraded. Examinations of the face and oral cavity may reveal the effects of intentional and unintentional injuries. With the results of the general assessment in hand, the clinician will classify the patient's general and oral health status and make treatment and/or referral recommendations.

A classification system adopted in 1962 by the American Society of Anesthesiologists, used to categorize a patient's risk on the basis of physical status, also has been applied, along with the patient's general and oral health risk assessment, to determine the need for coordinated multidisciplinary referral and whether care in a hospital is indicated rather than in the dental office (Bricker et al. 1994) (Table 8.3).

back to top

Changing Approaches to Selected Diseases and Conditions

The science and technology base is providing new approaches to risk assessment, diagnosis, prevention, and treatment. Highlights of selected diseases and conditions follow.

Dental Caries

Dental caries is caused by a transmissible microbial infection that affects tooth mineral. A number of factors play a role in the initiation and progression of the disease, including bacterial biofilm, specifically the presence of mutans streptococci and species of lactobacilli; the frequency of simple sugars in the diet; the flow and composition of saliva; the availability of fluoride; the structure of tooth mineral in a given individual; and oral hygiene behaviors. Sound caries management takes all these factors into account (Figure 8.3) (Burt and Ismail 1986). Today there is the prospect that clinicians will be able to balance protective and pathologic factors and work with the patient to control disease (Anderson et al. 1993, Edelstein 1994, Featherstone 1996).

Risk Assessment. Reviews of caries risk prediction models conclude that clinical variables, especially past caries experience, are the best predictors of new caries experience (Newbrun and Leverett 1990, Powell 1998). Table 8.4 shows a timeline summarizing the strongest predictors of caries incidence based on a review of the modeling literature. At the time of initial tooth eruption, the presence of mutans streptococci appears to be the primary predictor of future caries. With continued tooth eruption, this variable disappears as a primary predictor and is replaced by the status of the most recently exposed or erupted tooth surface. For example, the presence of carious lesions in the primary incisors has been found to be the best predictor of caries in the later-erupting primary molars (Powell 1998).

Despite recent declines, dental caries is a prevalent disease, with some age and population groups particularly vulnerable (see Chapter 4). A guide for the identification of vulnerable patients and the treatment of caries as an infectious disease has been developed (ADA 1995). Figure 8.4, from that guide, proposes questions to be considered at an initial examination. These questions, together with information gathered at recall examinations, allow classification of child and adult patients into high-, moderate-, and low-risk disease categories (Table 8.5). This approach has been incorporated in a variety of caries risk assessment forms adopted by some dental schools and managed care programs (C.W. Douglass, personal communication, 1999). Studies are needed to determine the validity and reliability of such approaches for different patient populations and practice settings.

The use of tests to assess caries risk to determine the activity status of preclinical disease is becoming more widespread. A range of diagnostic aids for caries activity testing are available. Microbial tests can detect the presence and quantify the levels of lactobacilli and mutans streptococci. The development and use of these tests are based on studies that have associated these microbes individually and together with different types of carious lesion development. Measurements of plaque and salivary pH have been used to evaluate the oral environment overall and to note the changes in pH that occur after eating various foods. Salivary flow and composition analyses add another dimension. Decreased flow has been related to caries susceptibility, as have increases in viscosity. These factors warrant further study to determine their sensitivity and specificity.

Diagnosis. Clinical signs, patient-derived history, and radiographic images remain the primary means of dental caries diagnosis. Tooth surface pitting and cavitation, white and/or brown spots, areas soft to tactile probing, and radiolucencies are used to detect the effects of this disease. The most common diagnostic approaches include visual inspection, the use of an explorer (a probelike instrument) to determine the integrity of the tooth surface, the use of a light source to detect difference in reflectance across tooth structure (transillumination), and radiographs. Table 8.6 compares the reported sensitivity and specificity of selected methods. No single method stands out as superior with regard to both sensitivity and specificity for all tooth surfaces.

The most basic diagnostic methods—visual alone and visual examination with an explorer—have limited sensitivity, but excellent specificity. The visual examination may be combined with a radiographic series for the initial assessment. Bite-wing radiographs are frequently used to diagnose interproximal caries (between teeth) and for these surfaces provide excellent sensitivity and specificity. Radiographic examination allows examination of otherwise inaccessible areas. Specifically, the depth of a lesion and its relationship to the pulp chamber can be evaluated for interproximal lesions. However, radiographs are of little value in detecting caries on the occlusal surfaces of the teeth. For these surfaces, a negative radiographic diagnosis does not imply lack of a carious lesion in enamel.

Precavitated carious lesions and caries in restored teeth pose an additional diagnostic challenge. A review of the literature on the clinical diagnosis of precavitated carious lesions concluded that visual detection of these lesions has low sensitivity and moderate specificity (Ismail 1997). It is difficult with these lesions to determine whether there is no caries or whether only the enamel or outer layer of dentin is involved. Carious lesions forming around restorations are seen more frequently at the approximal and cervical margins of these restorations (Mjör 1985). Distinctive color changes around a restoration alone are not diagnostic of active caries (Kidd 1990).

Currently, the progression of carious lesions is the most definitive diagnostic parameter for disease activity. Progression can be determined over specific time intervals only by professional assessment.

Prevention. The primary prevention of dental caries starts with adequate prenatal and perinatal nutrition to ensure normal development of the teeth and supporting structures. It continues with interventions aimed at preventing transmission of cariogenic microbes from caregivers to infants, and proceeds with specific strategies employed across the life span. These approaches include the provision of sufficient fluoride, the use of dental sealants, the adoption of healthy behaviors, including avoiding unhealthy dietary practices and practicing appropriate oral hygiene, and the timely use of care services. Although many factors are brought to bear on the primary prevention of dental caries, the combination of fluoride in its multiple forms and dental sealants is the foundation (as described in Chapter 7).

Fluoride is available in a variety of products that can be used by health professionals, individuals, and public programs. Topical solutions and gels, mouthrinses, and dentifrices are available for daily, weekly, or as-prescribed frequency. In addition, fluoride-containing prophylactic pastes are available for professional application (see Chapter 7). Clinical judgment of risk factors determines the type and frequency of interventions needed. Although there is general agreement on the overall value of topical fluorides in reducing dental caries (ADA 1986, 1994, Moss 1976, Stookey et al. 1993), comparative clinical trials are needed to determine which of the existing fluoride formulations (acidulated phosphate fluoride, stannous fluoride, amino-fluoride, or sodium fluoride) and which delivery system (gel, varnish, dentifrice, or solution) are most efficacious.

A second line of defense is through control of the etiologic agent. Chemotherapeutic agents (including the antimicrobial mouthrinse agent chlorhexidine and fluoride) can be used to reduce plaque. Dietary measures aimed at reducing the frequency and quantity of sugars and the substitution of sugars by sugar-free sweeteners may effectively starve the bacteria.

The process of tooth demineralization and re-mineralization has received significant attention over the past four decades (Geiger et al. 1992, Koulourides et al. 1961, Larsen and Fejerskov 1987, Linton 1996, Silverstone et al. 1981, White 1988), although the concept was documented in the early 1900s (Head 1912) (see Chapter 3). Investigators are studying the effectiveness of therapeutic agents for arresting carious lesions and remineralizing enamel in populations at high risk for dental caries. For example, a combined chlorhexidine-fluoride solution can enhance remineralization of incipient lesions and arrest caries in patients who suffer from radiation-induced caries (Katz 1982). The use of a twice-daily rinse with 0.05 percent sodium fluoride to prevent demineralization and induce remineralization in subjects with radiation-induced hyposalivation has also been found to be effective (Meyerowitz et al. 1991). This study also addressed the effects of chlorhexidine use alone, which has been associated with tooth staining, alterations in taste, and potential hypersensitivity reactions (Ohtoshi et al. 1986, Okano et al. 1989). Schaeken et al. (1991) showed that the application of 40 percent by weight chlorhexidine varnish every 3 months enhanced remineralization of root caries more than fluoride varnish, although both treatments were associated with fewer filled root surfaces than the control group after 1 year. A chlorhexidine varnish has not yet been approved in the United States, and large-scale, double-blind, placebo-controlled clinical trials are not yet available to test the effects of specific regimens in relation to caries risk.

Studies also are evaluating interventions to prevent mutans streptococci transmission. Findings from cross-sectional studies indicate that infants are initially infected by their parents, specifically mothers, around the time the teeth erupt (Berkowitz et al. 1975, Caufield et al. 1993, Kohler and Bratthall 1978). A longitudinal study using DNA fingerprinting demonstrated that mothers were the source of the bacteria in their infants and the degree of matching to maternal strains was higher for female infants than for males (Li and Caufield 1995). Based on a study of child-mother pairs (with the child initially at 1 year of age), the application of a 1.0 percent chlor-hexidine rinse alternated with a 0.2 percent sodium fluoride gel to the mother's teeth (3 times per day on 2 consecutive days, twice per year for 3 years) delayed, and in some cases prevented, the colonization of their children's teeth by mutans streptococci (Tenovuo et al. 1992). Timing of colonization has been shown to be correlated with caries prevalence. In a longitudinal study that followed children in 4-month intervals from 15 months to 4 years of age, children who were infected earlier had a higher caries prevalence than those in whom the infection was detected at later ages. Studies also have been aimed at reducing the levels of cariogenic bacteria in the infants themselves.

Work continues on the development of a caries vaccine. One approach focuses on the production and release of antibodies against cariogenic bacteria antigens (Russell et al. 1995). Specific antigens have been purified and synthesized. Another approach involves biological replacement therapy, where nonpathogenic bacteria, instilled in the mouth, prevent pathogenic bacteria from colonizing (Hillman et al. 2000). Yet another approach employs passive immunization in which antibodies, produced outside the body (in cultures, animals, eggs, or plants), are applied to the teeth and oral tissues to protect against disease. A recent study indicated that "plantibodies" painted on the teeth could prevent mutans streptococci colonization for 120 days, the period of the experiment (Ma et al. 1998).

Treatment. Prompt treatment of early carious lesions permits the preservation of tooth structure through conservative approaches. A 10-year study reported that caries did not progress under a dental sealant placed over cavitated lesions where the lesions were no more than halfway through the dentin (Mertz-Fairhurst et al. 1998).

Materials that can bond to enamel and to dentin continue to be refined and improved. Glass ionomer cements have contributed to materials that can bond to enamel and dentin, release fluoride, and increase remineralization in adjacent teeth (Mount and Hume 1998, Qvist et al. 1997). These cements, together with polymeric resin composites and hybrids of these two materials, are now available for tooth restoration with other materials. Based on the available materials and emerging techniques, such as air abrasion and laser ablation (Featherstone et al. 1998, Kantorowitz et al. 1998), restoration procedures are more conservative than ever before (Mount and Hume 1997).

A proposed categorization of carious lesions for the purpose of conservative management places lesions into three categories: lesions where no treatment is advised, lesions where preventive care is advised, and lesions where restorative treatment is advised (Pitts and Longbottom 1995). This approach, using caries as an infectious disease paradigm, resulted in a marked reduction of operative procedures in Danish schoolchildren (Thylstrup et al. 1995) and has been proposed as a means to preserve tooth structure and maximize appropriate care in the United States (Ismail 1997).

New imaging and laser technologies are emerging as tools for early diagnosis and prompt treatment of dental caries. For example, quantitative light-induced fluorescence is showing promise (de Josselin de Jong et al. 1996) for dental caries diagnosis. Two different methods, the quantitative infrared laser fluorescence method and electrical conductance measurements, are currently commercially available. At present, these methods are being used to augment conventional diagnostic tools but are not yet part of routine practice. However, they could potentially be used for close monitoring of the lesions and for patient motivation (Angmar-Månsson et al. 1996). Laser treatments for soft tissue surgery have been used in dentistry in recent years. Currently, in vitro studies are under way for the application of lasers for hard tissues, specifically to prevent dental caries by altering tooth mineral and inhibiting progression of artificial caries-like lesions (Featherstone et al. 1998, Kantorowitz et al. 1998).

Despite the best efforts of the individual and health care provider, caries may progress. Advances in materials science over the last two decades have fortunately led to major improvements in dental restorative materials, resulting in a wide range of aesthetically pleasing, longer-lasting restorations that can be placed with less trauma. Traditional materials such as amalgam fillings and gold crowns are now augmented by aesthetic materials, including bonded composite resins, porcelain fused to metal crowns, and facings.

When teeth have been lost, the options for rehabilitation include a range of prosthetic devices. Removable full and partial dentures and fixed bridges provide aesthetic and serviceable restorations for many patients. Still another option is the use of dental implants. These are used not only in patients who have lost teeth due to caries and periodontal diseases, but also to restore form and function in patients treated for trauma, craniofacial cancers, hereditary tooth defects, and other abnormalities.

The evidence base for the survival of the endosseous dental implants, an implant that is placed directly into a tooth socket, is extensive and has been recently reviewed (Cochran 1996, Fritz 1996). The predictability of endosseous dental implants in fully and partially edentulous patients has been clearly demonstrated in longitudinal studies (Albrektsson 1988, Albrektsson et al. 1988, Buser et al. 1991, Spiekermann et al. 1995). Many implant designs and surfaces have shown high success rates (often exceeding 95 percent in good-quality bone and 85 percent in poorer-quality bone, such as the posterior maxilla) (Buser et al. 1988, Cochran 1996, Fritz 1996).

Rehabilitation of lost tooth structure or even the whole tooth itself may be revolutionized in the next century, based on discoveries of the natural repair and regeneration mechanisms the body uses. The new sciences of biomimetics and tissue engineering combine engineering principles and materials science with rapidly growing knowledge of the progenitor cells and molecules that give rise to specific tissues such as skin, bone, teeth, and cartilage. Already it is possible to generate new cartilage and bone of a prescribed shape to replace tissue lost from injury or disease (Reddi 1995). Eventually, it may be possible to use a patient's own oral cells and cell products to generate new tooth enamel, dentin, and cementum for the natural repair of carious lesions.

Periodontal Diseases

Periodontal diseases are caused by microbial infections, and are plaque-related complex diseases like dental caries, presenting as several clinical variants (see Chapter 3). The mildest form is gingivitis, characterized by inflammation of the gingiva with a marked loss of gingival collagenous material (Page and Schroeder 1976, Schroeder et al. 1973). In a more advanced disease, periodontitis, there is involvement of the soft tissue and bone that support the teeth. If untreated, periodontitis may progress and result in abscesses, mobile teeth, and tooth loss. Periodontitis also may be associated with certain systemic diseases and conditions (see Chapter 5).

Gram-negative anaerobic bacteria in plaque are implicated as causative agents in periodontitis. However, host immune system factors, specifically, a chronic inflammatory response, are now considered to be the primary determinants of disease progression and outcome (Page 1998). The disease process is very similar across the different types of periodontal disease and involves interactions between infectious agents and their virulence factors and host defense mechanisms, operating within a context of environmental, acquired, and genetic risk factors specific to a given individual. Figure 8.5 illustrates the pathogenesis of these diseases (Page and Beck 1997).

Risk Assessment. Sufficient knowledge of demographic and systemic risk factors and indicators has been acquired to guide clinical decisions in the management of periodontal diseases (Genco 1996, 2000, Page and Beck 1997, Papapanou 1998). Table 8.7 provides an overview of the strength of the associations of local and systemic factors with destructive periodontal diseases (Genco 1996, 2000). Table 8.8 presents the odds ratios derived from studies that investigated the likelihood of developing periodontal disease given a specific risk factor, indicator, or marker/predictor (Jeffcoat et al. 1997, Page and Beck 1997). The presence of pathogenic bacteria, poor oral hygiene, tobacco smoking, diabetes mellitus, and preexisting periodontal disease are some of the factors that contribute to the likelihood of disease presence, progression, and treatment outcomes.

A systematic identification of risk factors, indicators, and predictors has been proposed as the first step in diagnosing and managing periodontal diseases (Genco 1996, Page and Beck 1997, Papapanou 1998). Clinicians can weigh the known risks for individual patients and devise treatment plans appropriate to their risk category. These same factors and the outcomes of treatment can also be used to assess prognosis upon completion of therapy. Studies are under way to determine the feasibility and validity of assessing a complex of risk factors to predict states of periodontal health and disease (Genco 1996, 2000, Genco et al. 1999, Papapanou 1998).

Most recently, putative genetic markers for susceptibility for oral disease have been studied. In particular, a specific genotype of the polymorphic IL-1 gene cluster has been shown to be associated with severe periodontitis in nonsmokers (Kornman et al. 1997). IL-1-beta is of interest because the proinflammatory cytokines are key regulators of the host immune response to microbial infection and extracellular matrix catabolism and bone resorption. Functionally, this polymorphism is associated with high levels of IL-1 production, and high levels of IL-1 have been associated with progressive periodontal breakdown (Cavanaugh et al. 1998).

A consensus has been reached by a specialty organization that all patients in general and specialty care should be screened for periodontal disease (AAP 1996). The recommended approach is to apply the Periodontal Screening and Recording examination (PSR). Related screening tests include the Community Periodontal Index of Treatment Needs (CPITN) (Ainamo et al. 1982) and the Basic Periodontal Examination.

Diagnosis. The strengths and weaknesses of the range of tests and methods used to diagnose periodontal diseases are presented in Table 8.9. Most diagnostic tests for periodontal diseases rely on a physical examination to note any swelling, redness, gingival bleeding, or tooth mobility. Periodontal probing, radiographs, and microbiologic and histological examinations of biopsied tissue provide important additional information. These tests indicate the presence, extent, and severity of gingival and periodontal tissue destruction; they do not indicate the cause of disease or whether it is quiescent or actively progressing.

Gingival inflammation may be assessed using a variety of methods, including bleeding on probing and the use of indices such as the gingival index (Löe and Silness 1963) to grade redness and bleeding. In adult periodontitis, the absence of inflammation is associated with a lack of disease progression, but the presence of inflammation does not indicate inevitable progression to destruction (Armitage 1996, Halazonetis et al. 1989, Okamoto et al. 1988). Longitudinal studies have also been conducted in patients who participate in maintenance programs. The absence of gingival bleeding, especially at recall visits, has been shown to be a valid indicator of gingival health in these patients (Lang et al. 1986).

Measurement of probing depths (also termed pocket depths) is an integral part of the periodontal examination. Longitudinal studies have shown that shallow probing depths and minimal loss of attachment are associated with lack of disease progression. The mere presence of a pocket does not herald progressive periodontitis at that site. Although teeth with moderate to deep probing depths are at higher risk for additional destruction, a single examination cannot determine the fate of the tooth with certainty (Armitage 1996, Haffajee et al. 1983, Halazonetis et al. 1989, Okamoto et al. 1988).

Radiographs are used to obtain a visual image of the bony support around a tooth or dental implant. They are an essential tool in planning complex prosthetic reconstructions, as well as a necessary diagnostic aid in assessing periodontal progression.

At least 15 different organisms have been associated with adult periodontitis. The 3 species most strongly linked are Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. Actinobacillus actinomycetemcomitans is most strongly linked to early-onset periodontitis (Haffajee and Socransky 1994). No single bacterial species has been shown to satisfy Koch's postulates (Moore 1987, Socransky and Haffajee 1992), leading some investigators to suspect that periodontitis is a mixed infection (Ranney 1993). As a result, diagnostic tests for periodontal diseases have included assessments of the presence and amount of several putative microbes in the subgingival plaque.

Routine bacterial testing of patients with adult periodontitis is not usually necessary and indeed is not supported by the preponderance of the evidence (Armitage 1996, AAP 1996). In formulating treatment programs for special patient populations and as a research tool, however, the tests can be very helpful. Such patients include those refractory to previous therapy, patients with rapidly progressive or early-onset periodontitis, and certain medically compromised patients.

The traditional method for assessing the subgingival flora is by culturing samples extracted from the site of infection. Culturing allows the clinician to determine the antibiotic sensitivity of the organisms, but it is technique-sensitive: scrupulous care is required when sampling the periodontal pocket. This is especially true for microbes that are strict anaerobes, because they are killed by even brief exposure to air. The requirement that bacteria have time to grow also precludes chairside testing.

With the advent of molecular biology, bacterial species can be identified by their DNA (Moncla et al. 1988, Savitt et al. 1988, 1990) or by unique antigenic components (Zambon et al. 1986). Either method will detect putative periodontopathic bacteria quickly and with a high degree of sensitivity and specificity, usually above 90 percent. The tests do not indicate whether there is actual disease, however. Nor do the tests reveal anything about the antibiotic sensitivity of the detected bacteria. Because DNA is very stable, the tests can be applied to nonliving plaque samples, simplifying the collection process. Kits are available that allow DNA testing to be performed in the dental office; otherwise the samples are sent to a reference laboratory.

Other tests are available for the detection of groups of putative periodontopathic bacteria (Loesche 1986). The BANA test detects a trypsin-like enzyme that is present in P. gingivalis, T. denticola, and B. forsythus (Loesche et al. 1990). Somewhat less accurate than the tests described above, the BANA test is 92 percent sensitive and 70 percent specific in detecting these groups of bacteria.

Once a periodontal infection is established, telltale metabolic changes occur in the body as a result of inflammation, injury, or death of tissue. A sample of fluid exudate from the gingiva (gingival crevicular fluid) in an affected pocket can be analyzed for these changes. They include elevated levels of prostaglandin E2 (Cavanaugh et al. 1998, Offenbacher et al. 1986), interleukin 1 and interleukin 6 (Cavanaugh et al. 1998, Geivelis et al. 1993, Masada et al. 1990, Tsai et al. 1995), tumor necrosis factor (Rossomando et al. 1990), beta-glucuronidase (Lamster et al. 1994, 1995), aspartate aminotransferase (Chambers et al. 1991, Persson and Page 1992), elastase (Armitage et al. 1994, Palcanis et al. 1992), and collagenase (Lee et al. 1995). Most of these analyses are based on inserting a filter paper strip into the isolated pocket to collect the fluid and testing for the metabolite of interest. A positive result usually indicates that inflammatory or destructive pathways have been triggered, but provides no clues concerning the etiologic factor or factors. Because of differences in experimental designs in the clinical studies, it is difficult to compare the sensitivity and specificity of each metabolite in detecting disease.

Prevention. Because periodontal diseases are plaque-associated infections, prevention and management of the early signs of these diseases depend on effective plaque control. This can be accomplished using both mechanical and chemotherapeutic approaches (Table 8.10). The prophylaxis performed in the dental office on periodontally healthy patients reduces plaque and removes stains and calculus. How often patients should be recalled for such preventive procedures is based on an assessment of risk factors such as the patient's age, oral hygiene, personal habits (e.g., smoking and diet), and a medical history indicating a heightened risk of infection (such as noted with diabetes or HIV infection) (Hancock 1996, Mealey 1996).

Chemical plaque control has become an important part of the clinician's armamentarium and may be prescribed for patient care at home (Table 8.10). Reviews of the literature by Hancock (1996) and Drisko (1996) provide detailed supporting evidence. Significant reductions in gingival inflammation have been demonstrated for chlorhexidine, triclosan co-polymer when used in conjunction with a fixed combination of essential oils, and stannous fluoride. The magnitude of gingival inflammation reduction was greatest for chlorhexidine. The evidence supporting these effects includes multiple randomized, double-blind, controlled clinical trials.

Treatment. Once periodontal disease is established, the resultant bone and connective tissue loss may be quiescent or actively progressing. The goal of treatment is to determine whether the disease is active in order to prevent further tissue loss. This entails professional plaque removal and careful instruction of the patient on scrupulous self-care.

The concept of management of a patient's risk factors as part of treatment is reasonably well documented for individuals who smoke and those who are diabetic and may be important for other risk factors such as stress (Genco et al. 1999) and low dietary calcium (Nishida et al. in press). Several studies have shown that treatment of periodontal disease in smokers is not as successful as in nonsmokers (Grossi et al. 1996). Thus, the management of smoking as a risk factor will contribute to the success of periodontal therapy. Furthermore, it appears that treatment of diabetic patients with periodontal disease may require more intense therapy since several studies have shown that antibiotic therapy is successful not only in reducing periodontal disease, but also in reducing glycated hemoglobin (Grossi and Genco 1998).

Professional plaque removal typically employs scaling and root planing, in which hardened deposits of plaque and other debris are removed from the periodontal pocket and the tooth root surface is smoothed over. The effectiveness of scaling and root planing has been demonstrated repeatedly in longitudinal, cohort, and randomized clinical trials and was reviewed by Cobb (1996). Demonstrated benefits include decreased gingival inflammation, decreased probing depth, and facilitation of maintenance of clinical attachment level. The evidence indicates that similar results may be obtained with ultrasonic and sonic instruments as with manual instruments. Regardless of the methods used, meticulous attention to detail is required to achieve optimal results (Cobb 1996).

Topical administration of antimicrobial agents contributes to the control of gingival inflammation (Table 8.10). Supragingival irrigation (e.g., applying a jet of water under pressure) may be used as an adjunct to toothbrushing and has been shown to aid in the reduction of gingival inflammation. However, no clear substantial long-term benefits for the treatment of periodontitis have been shown if irrigation is applied subgingivally.

Surgical therapy is employed to provide access to root surfaces and bony defects for debridement and root planing. Surgery can facilitate regeneration, augment the gingiva, and promote root coverage (Table 8.11). It is also necessary in placing dental implants.

Palcanis (1996) reviewed the evidence regarding surgical therapy. The overall goal is to make plaque control easier for the patient, thereby reducing disease progression. Many surgical techniques are available. Extensive randomized clinical trials and longitudinal studies form the basis of the evidence for the efficacy of these procedures (Kaldhal et al. 1996, Knowles et al. 1979, Pihlstrom et al. 1983, Ramfjord et al. 1987). All procedures decrease pocket depth, and, with the exception of gingivectomy, all increase clinical attachment level. A caveat to be noted, however, is that procedures designed to reduce probing depth may increase gum recession, exposing the root and possibly compromising aesthetics. Thus, selection of a particular surgical procedure must always be based on the individual needs of the patient. Regardless of the approach selected, maintenance is important to long-term success.

Systemic administration of antibiotics, including the tetracyclines,3 metronidazole, spiromycin, and clindamycin, has been extensively studied and reviewed (Drisko 1996). The risk of generating antibiotic resistance in bacteria precludes the use of systemic agents in treating simple gingivitis (AAP 1996). Similarly, systemic antibiotics should not be used for the routine first-line treatment of common forms of adult periodontitis (AAP 1996, Drisko 1996). The preponderance of evidence from well-controlled, randomized, blinded clinical trials indicates that the agents do not offer sufficient benefit to overcome risks of either drug sensitivity or the emergence of antibiotic-resistant pathogens.

The situation is different in cases of aggressive forms of periodontitis, such as early-onset, rapidly progressive, or refractory periodontitis, which affect less than 10 percent of periodontitis patients. Randomized, double-blind clinical trials, as well as longitudinal assessments, indicate that the use of systemic antibiotics can slow disease progression in these patients (AAP 1996, Drisko 1996).

To circumvent the problems of systemic therapy, investigators have applied antimicrobial agents directly into the pocket. Antimicrobials incorporated into either resorbable and nonresorbable interpocket delivery systems have been studied in randomized, double-blind, controlled clinical trials and are now FDA approved and on the market (Goodson et al. 1991, Jeffcoat et al. 1998). When used as an adjunct to scaling and root planing, gains in clinical attachment level and decreases in probing depth and gingival bleeding were demonstrated. Because these delivery systems are relatively new, there is a paucity of evidence addressing their long-term effectiveness.

For patients who have lost significant bone and/or connective tissue, there are a number of regeneration procedures to facilitate the growth of new periodontal ligament, cementum, and alveolar bone over previously diseased root surfaces. The evidence base for bone-grafting techniques using either natural or synthetic bone materials has been reviewed by Garrett (1996). Natural bone grafts may use autografts, in which bone is transferred from one site to another in the same patient; allografts, which use bone grafts from a human donor; and xenografts, which use tissues from other species. Limited case report evidence shows that extraoral autogenous bone, such as hip grafts, has high potential for bone growth (Garrett 1996). Extraoral sites require a second surgical site, and in some cases fresh grafts may be associated with root resorption. Case report evidence indicates bone fill exceeding 50 percent of the osseous defect may be achieved (Garrett 1996). Controlled studies comparing grafted to nongrafted sites report significant improvements in clinical attachment levels and bone gain, but the magnitude of gain is less than that indicated in case reports.

Freeze-dried demineralized bone represents one of the most frequently used and well-studied bone graft materials in periodontics. Freeze-dried demineralized bone is an allograft material, harvested, prepared, and demineralized prior to grafting. The demineralization step is important because it retains the activity of bone morphogenetic proteins—compounds in the graft material found to be essential for new bone formation (Urist 1965, Urist and Iwata 1973). Case reports and controlled clinical trials have demonstrated the bone-forming potential of such material, with some variability in the amount of bone fill achieved (Garrett 1996). Because allografts are derived from donor tissues, proper collection, handling, and storage are essential to ensure viability and prevent contamination with viruses or other pathogens (Mellonig 1995).

Alloplasts represent a class of synthetic resorbable or non-resorbable graft materials. When evaluated in controlled clinical trials, they demonstrated improvements in probing depth and attachment level (Garrett 1996). Histology, however, indicates that, in general, synthetic grafts act primarily as space fillers, with little, if any, regeneration.

Beginning in the 1980s a number of investigators explored a procedure called guided tissue regeneration. The idea was to employ either a resorbable or non-resorbable membrane at the diseased site that would selectively allow passage of cells able to regenerate periodontal attachment apparatus and bone, while prohibiting migration of non-regenerative cells such as fibroblasts. The evidence for the efficacy of guided tissue regeneration ranged from randomized controlled clinical trials to case reports (Garrett 1996). Although less evidence is available for resorbable membranes than for non-resorbable membranes, significant improvements in clinical attachment levels have been shown compared to debridement alone. Most favorable results are reported for bone loss between the roots of mandibular tooth defects (Class II furcations). Less favorable results were reported in maxillary molar and Class III (through and through) furcation defects (Garrett 1996).

Oral and Pharyngeal Cancers

Oral and pharyngeal cancers, like other neoplastic diseases, are caused by mutations in cell regulatory genes. The mutations contribute to carcinogenesis by promoting uncontrolled cell growth, suppressing the function of tumor suppressor genes, promoting the growth of new blood vessels (angiogenesis) to nourish the growing tumor, or facilitating metastasis. A model depicting the genetic progression for oral and pharyngeal cancers has been proposed (Califano et al. 1996).

Potentially malignant lesions can present in a variety of ways and can include erythroplakia or leukoplakia (red or white flat lesions, respectively), ulceration, failure of a wound to heal, lymphadenopathy, induration, dysphagia, and tissue growth. Erythroplakia lesions are considered to have a higher rate of malignancy than leukoplakia (Silverman 1990). Candida albicans infection of a leukoplakia lesion appears to increase the risk of malignant transformation (Field et al. 1989, Scully 1995). In addition, infections with strains of human papillomavirus (HPV) and herpes simplex virus (HSV) have been implicated in the etiology of oral cancers. Other potentially predisposing factors include chronic iron deficiency anemia, erosive lichen planus, oral submucous fibrosis, and actinic keratosis.

Risk Assessment. Risk assessment for oral and pharyngeal cancers (Table 8.12a) includes an evaluation of the patient's exposure to tobacco and alcohol and an examination to identify suspicious lesions and conditions thought to predispose to cancer. All tobacco products (see Chapters 3 and 10) have been associated with oral and pharyngeal cancers. The risk of oral cancer is increased 6 to 28 times in current smokers. Alcohol is also a risk factor for oral cancer, and combined with tobacco use accounts for 75 to 90 percent of oral cancer in the United States (Blot et al. 1988, Vokes et al. 1993). A dose-response relationship has been demonstrated for cigar smokers, and the overall risk of cancer is 7 to 10 times higher among users than for those who never smoked (NCI 1998). In addition, individuals who have had oral cancer are at increased risk for a second primary cancer, and this risk is higher than that for other cancers (Boice et al. 1985, Winn and Blot 1985).

Other factors, such as infection with HPV or HSV, as noted earlier, and use of high-alcohol-content mouthwashes, also have been associated with oral cancers (Flaitz and Hicks 1998, Sugerman and Shillitoe 1997, Winn et al. 1991). Lip cancer is associated with exposure to the sun (Pogoda and Preston-Martin 1996).

Biomarkers—measurable alterations in molecules derived from human tissues or fluids—are being developed to identify those at risk for oral cancer and to identify which patients may benefit from specific treatments (Lippman et al. 1993, Patterson et al. 1996, Sidransky 1997). These markers may also be able to predict oral cancer recurrence or the occurrence of new primaries (Shin et al. 1996).

Diagnosis. At present, the diagnosis of oral and pharyngeal cancers involves a systematic extra- and intraoral physical examination to identify lesions and conditions that may be precancerous or indicate a predisposition to cancer (USDHHS 1998). Biopsies are essential to confirm the clinical observations. The sensitivity and specificity of a brush biopsy have been established in a multisite clinical trial (Sciubba 1999). Imaging technology may also be employed to determine the extent of the lesion. Although the sensitivity and specificity of the physical examination have not been established in clinical studies, it is clear that persons with localized oral and pharyngeal cancers have a better prognosis than persons whose cancers were detected with regional or distant spread (Ries et al. 1999). A thorough examination for oral and pharyngeal cancers is recommended by the American Cancer Society annually for individuals over 40 and for individuals who are exposed to known risks (Murphy et al. 1995).

Prevention. Primary prevention of oral and pharyngeal cancers involves avoiding known carcinogenic agents (Blot et al. 1988, Vokes et al. 1993), primarily tobacco in any form and excessive use of alcohol. In addition, the use of lip balms with ultraviolet radiation blockers is recommended (see Table 8.12b). A high dietary intake of fruits and vegetables may reduce oral and pharyngeal cancer risk by as much as 30 to 50 percent (McLaughlin et al. 1988). Dentists, physicians, and nurse practitioners among others are in a critical position to counsel patients on tobacco and alcohol use, pointing out that tobacco cessation lowers the risk for oral and pharyngeal cancers (Blot et al. 1988). Physicians, dentists, and other health care professionals have been shown to be effective in increasing tobacco cessation rates (Cohen et al. 1989, Ockene et al. 1991, Stevens et al. 1995, Wilson et al. 1988). A prime reference for use in national and international antismoking efforts is the Clinical Practice Guideline on Smoking Cessation (Number 180) developed by the Agency for Health Care Policy and Research (Fiore 1997).

Treatment. Diagnosis of cancer at an early stage can be followed by prompt and conservative treatment of the affected tissues. Some early lesions may be successfully treated with excisional biopsy; more advanced cases will require additional surgery, radiation, and/or chemotherapy (Shah and Lydiatt 1995, Vokes and Athanasiadis 1996). Preservation of function and appearance is emphasized. Advanced cancers require follow-up reconstruction and rehabilitation to improve function and aesthetics.

Birth Defects

There are hundreds of genetic diseases and syndromes as well as congenital anomalies that affect the craniofacial, oral, and dental tissues. However, some craniofacial anomalies may be spontaneous and manifest only at the time of birth. Chapter 3 describes a number of these disorders. Rapidly advancing knowledge of the genetics of development and of mutations associated with specific birth defects is aiding in the development of screening tests for genetic disorders and identifying high-risk individuals and families.

A complete diagnosis of the craniofacial disorder may involve a multidisciplinary team of experts in imaging, genetics, and other areas. Similarly, long-term management of the disorder, often extending to adulthood, generally calls for a team of specialists, including physicians and dentists, surgeons, nurses, rehabilitation experts, speech pathologists, psychologists, and social workers. Quality of life considerations, including social and psychological effects of birth defects such as cleft lip and palate, are taken into account (see Chapters 3 and 6).

Prevention. Primary prevention involves minimizing exposure to known teratogens, and genetic counseling as appropriate. The importance of educating parents or potential parents on behavioral risk factors, especially tobacco and alcohol use, the teratogenic potential of certain prescription drugs, and the need for adequate nutrition in the perinatal period is emphasized. In a study by Tolarova and Harris (1995), supplementation of the diet by multivitamins and folic acid during the periconceptional period (i.e., before, during, and after conception) markedly diminished the occurrence of cleft lip and palate in a high-risk group. Unfortunately, only about 29 percent of women of childbearing age consume recommended amounts of these essential nutrients (Werler et al. 1999). The evidence associating moderate to severe periodontal disease in pregnant women with low-weight preterm births warrants attention to the importance of maintaining optimal oral health in pregnancy. The oral care clinician can contribute to birth defect prevention not only by treating oral disease, but also by providing educational messages to patients to promote the birth of healthy, full-term babies.

Treatment. A number of birth defects may not be apparent at birth because they are not manifested until later in development. One example is the ectodermal dysplasias (EDs), disorders characterized by abnormalities of skin, hair, sweat glands, and teeth. Dentists are essential in the management of care for children with these disorders, who must be repeatedly fitted with dentures throughout childhood. More recently, clinical studies have demonstrated that fitting ectodermal dysplasia patients as young as 12 years old with dental implants not only is effective, but also provides greater functional utility and satisfaction (Guckes et al. 1998, Kearns et al. 1999). As with other complex craniofacial anomalies, management by a multidisciplinary team is the best approach, with experts able to advise on the various oral, skin, and sweat gland complications.

Mutations have recently been identified for several forms of ED, including the anhydrotic form (absence of sweat glands). Ultimately, the development of genetic diagnostic tests can confirm the diagnosis in the child and permit counseling of parents.

back to top

Chronic Craniofacial Pain and Sensorimotor Conditions

A variety of problems involving pain and other sensorimotor abnormalities affect the craniofacial complex. These conditions can include burning mouth syndrome, trigeminal neuralgia, various facial palsies, postherpetic neuralgia affecting branches of the trigeminal nerve, temporomandibular disorders, fibromyalgia, and disorders of taste or olfaction. Some of these are infectious in origin (e.g., postherpetic neuralgia and some taste disorders); some are traumatic (e.g., some cases of temporomandibular disorder); and for others, the cause or causes are unknown (see Chapter 3). Patients with facial palsies and trigeminal neuralgia are generally referred to neurologists for treatment. Disorders of taste and smell also require neurological consultation as well as brain imaging because they can be symptomatic of brain tumors.

Pain relief may also improve function and can be combined with adjunctive measures such as the use of hot or cold compresses and behavioral treatments such as relaxation and imaging therapy to reduce muscle tension. The variety of pain medications has greatly increased in recent years. They include aspirin and other nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, new antiepileptic drugs, the selective serotonin re-uptake inhibitors, and the more potent opiate family of drugs.

If the pain problem has recently developed, providers take steps to prevent the pain from becoming chronic. This will entail a general health assessment to determine whether there are co-morbidities, including other pain problems, as well as patient questionnaires to provide information on how the pain problem is affecting overall health and well-being. The data collected will record the extent to which the problem interferes with work, social interaction, and sleep, whether the patient is experiencing mood changes and symptoms of depression, and what coping skills are manifest. Such patient profiles allow for more selective treatment tailored to the needs of the individual patient.

Patients in whom pain has become chronic and intractable may be referred to an established pain clinic for multidisciplinary treatment and may also be alerted to patient organizations where individuals with similar pain problems can find information and support.

back to top

Temporomandibular Disorders

Among the common types of craniofacial pain likely to be seen by oral care providers are temporomandibular disorders, characterized by symptoms of pain and dysfunction in and around the temporomandibular joints or the masticatory muscles.

Temporomandibular disorders may occur as a result of injury, arthritis, or fibromyalgia or for unknown reasons. Approaches used to obtain a differential diagnosis of these conditions can range from a physical examination that may include palpation and measuring the mouth opening, to the use of complex imaging and instrumentation, including procedures such as arthroscopy (Table 8.13) (Clark et al. 1993, NIH 1996, Rao 1995, Rao et al. 1990).

Diagnosis of temporomandibular disorders is based on the physical examination and a complete medical and dental history, including information about hearing, speech, and swallowing problems, as well as pain and dysfunction. This information can be complemented by data from imaging and other diagnostic tests (Clark et al. 1993, NIH 1996). Evaluation encompasses examination of oral-facial tissues, musculature, and neurological function.

Particular attention is paid to measures of the range of motion, mouth opening, existence of any parafunctional conditions (e.g., clenching, grinding), and the presence of joint or muscle tenderness and cutaneous hyperalgesia. Features of the reliability studies on the examination methods have been reviewed (Clark et al. 1993, Mohl et al. 1990). Psychosocial assessments using validated instruments can determine the extent to which pain and dysfunction diminish the patient's quality of life (Dworkin 1994) and can suggest appropriate treatments (NIH 1996, Travell and Simons 1983, Zarb 1994).

The evidence base for the efficacy of treatment modalities is severely limited and has resulted in a wide range of diagnostics and therapies. Treatments range from conservative and reversible approaches to joint surgical procedures. At present the evidence is insufficient to warrant prophylactic intervention for management of these disorders (NIH 1996).

Currently available epidemiological evidence suggests that temporomandibular disorders can frequently resolve over time and that conservative, reversible approaches are the treatments of choice. Ideally, the practitioner and the patient should work together to develop a treatment plan that is evidence-based and patient-centered, taking into consideration all etiologic factors, the level of pain and dysfunction the patient is experiencing, and their impact on the patient's quality of life (see Chapter 3).

back to top

Mucosal and Autoimmune Diseases

Microbial infections and autoimmune disorders contribute to a range of mucosal and gingival conditions. The physical examination may be sufficient to identify the lesions associated with herpes virus infections (cold sores), papillomaviruses (oral warts), or fungal infection (commonly, infection by Candida albicans), with definitive diagnosis confirmed by cytology, biopsy, culture, or in situ hybridization. The patient's history and immune status can supply additional information indicating risk factors, including the presence of systemic diseases. Selected major mucosal diseases and associated clinical findings are described in Chapters 3 and 5. Tissue biopsy is critical for the diagnosis of many mucosal diseases. In addition, oral sites may be convenient biopsy sites for autoimmune diseases such as Sjögren's syndrome, which have both a systemic and an oral-facial component. Although the evidence base in terms of randomized, double-blind, controlled clinical trials for the treatment of oral manifestations of mucocutaneous disorders is limited, treatment options generally depend on the severity and extent of the disease. Because many of the available drugs may have significant side effects, evaluation of the risk-benefit ratio for the patient is always of great importance. Coordination of care with other health care providers is warranted.

back to top


The last decades of the twentieth century were witness to major improvements in the prevention, diagnosis, and treatment of oral diseases—a trend that will continue to accelerate the paradigm shift in the management of oral diseases from repair of damaged tissues to the control of infections. In addition, modification of risk factor exposures will result in improvements in health and in the management of disease. A closer look into factors that will affect the future of oral health care requires an overview of the current state of guidelines for oral care and the status of evidence-based practice. The approaches used to determine the evidence for practice and the development of guidelines for care are an emerging field of activity. Education in the health professions is already emphasizing the importance of relying on randomized, controlled clinical trials, the gold standard for judging the merits of proposed interventions, wherever possible.

back to top

Evidence-based Practice

During the 1990s, "evidence-based medicine" emerged as both popular phraseology and practice philosophy. The origins of evidence-based medicine go back to mid-nineteenth-century Paris and earlier, yet the approach is still a relatively young discipline that is now rapidly evolving (Sackett et al. 1996). Evidence-based medicine has been defined as the integration of "individual clinical expertise with the best available external clinical evidence from systematic research" and with patients' choices (Sackett et al. 1996). The skills required include defining a clinical problem, critically appraising the relevant literature, and deciding whether and how to integrate this information into practice (Evidence-Based Medicine Working Group 1992). Evidence-based medicine is neither a "cookbook" nor an ivory tower approach (Sackett et al. 1996).

The philosophy is being adopted across a range of disciplines, leading to the terms "evidence-based dentistry" and "evidence-based nursing," among others. The practice of evidence-based dentistry "incorporates the judicious use of the best evidence available from systematic reviews, when possible, with knowledge of patients' preferences and clinicians' experiences to make recommendations for the provision of the right care, for the right patient, and at the right time" (Ismail et al. 1999).

The reliance on evidence using systematic reviews of the literature has led to initiatives in the United States, Canada, and Europe to enhance the conduct and use of systematic reviews. The Agency for Healthcare Research and Quality (AHRQ) created 12 evidence-based practice centers in 1997 to conduct systematic reviews and develop evidence reports. The Cochrane Collaboration and the Centre for Reviews and Dissemination at the University of York are examples of prominent activities in the United Kingdom to support systematic reviews. The Cochrane Oral Health Review Group, one of 50 specialty review groups within the Cochrane Collaboration, has a number of systematic reviews completed or under way of interest to oral health practitioners (see Table 8.14) (Tavender 1999). In Canada, considerable contributions to the field have been made by McMaster University and the Canadian Coordinating Office for Health Technology Assessment.

In the United States, the National Institute of Dental and Craniofacial Research joined efforts with AHRQ in 1999 to designate one of AHRQ's Evidence-based Practice Centers to conduct reviews on oral, dental, and craniofacial diseases and disorders. The work of this center should significantly strengthen the scientific base of knowledge related to the diagnosis and management of oral, dental, and craniofacial conditions. Examples of topics that will be reviewed include the management of dental caries, and dental care of medically compromised patients, including patients with HIV disease.

back to top

Clinical Practice Guidelines

The development of clinical practice guidelines is one of the intended outcomes of evidence-based reviews. The classic definition for clinical practice guidelines describes them as "systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances" (Field and Lohr 1992). A 1995 review of the status of clinical practice guidelines in dentistry (Shugars and Bader 1995) found that a limited number of guidelines were available and that few extant guidelines met all of the des-irable attributes for guidelines identified by the Institute of Medicine (Field and Lohr 1992). Most notably, a majority of guidelines were based on consensus among selected professionals, with little evidence of support from the scientific literature. Since 1995, the number of dental practice guidelines has grown slowly but steadily. Table 8.15 lists selected sets of guidelines that, taken together, represent an estimated 50 percent of all current published dental guidelines intended for national distribution. When 36 national dental organizations representing clinical aspects of dentistry and dental practice were surveyed in early 1999, 12 of 22 responding organizations indicated that they had developed guidelines (J.D. Bader, personal communication, 1999), 8 of which are listed in the table. Some of these guidelines have not been widely distributed, are not published in the scientific literature, nor are available on the sponsoring organization's Web site. Not shown are guidelines developed by care delivery organizations for use in their clinical practices. These are generally not available for public or external professional scrutiny.

The table provides information on two important characteristics of clinical practice guidelines: the extent to which they are evidence-based and their level of specificity, which will determine their clinical applicability. Clinical applicability is a key feature of practice guidelines, and it is heightened as the amount of specific information in a guideline is increased to identify patient and condition characteristics to which the guideline applies. As the "evidence-based" concept gains popularity, there is a growing expectation that clinical practice guidelines will reflect systematic evaluation of the relevant literature and will present an evaluation of the strength of the evidence for each recommendation (Ismail et al. 1999). Such information, which ensures the content validity of the guidelines, not only helps practitioners and patients understand exactly what is and is not known about the effectiveness of proposed treatments, but also identifies research needed to evaluate current practice. A less comprehensive but still useful approach to identifying the scientific support for clinical interventions is the traditional approach of citing specific studies and reviews when discussing specific treatments. Practice guidelines without explicit linkages to the literature, such as those supported only by selected citations not linked to specific statements and those without any citations, can still be useful, but users have less assurance that the content is valid.

As the expectations for the content and use of clinical practice guidelines mature, "perhaps the main task of guideline development [will be] to summarize the strength of the evidence for the effectiveness of a given clinical practice in relation to risks and costs" (Fletcher and Fletcher 1998). Thus, practice guidelines will need to be revised considerably to incorporate the literature on treatment outcomes as they become available. Currently, information on both the effectiveness of specific dental treatments and the range of outcomes examined is extremely limited (Bader and Shugars 1995). For example, none of the guidelines in the table address patient preference or patient utility issues. Dental organizations have the opportunity to address these information gaps as practice guidelines are developed. Professional dental organizations are the most likely developers, but other organizations can also be vigorous participants. Finally, organizations developing guidelines should also develop a plan for their dissemination, evaluation, and revision. The existence of guidelines does not ensure that appropriate treatment decisions will be made. Passive distribution of clinical practice guidelines is generally ineffective in altering practice, whereas more active, multifaceted interventions can achieve some measure of desired change (Bero et al. 1998).

back to top

Science and Technology Contributions

During the past several decades, there have been major improvements in the prevention, diagnosis, and treatment of oral diseases. Enhanced disease prevention and health promotion will require the participation of all health professions, especially in addressing common risk factors such as tobacco, alcohol, and inappropriate dietary practices. The field of diagnostic tests for oral diseases should continue to expand, enabling clinicians to analyze the risk of disease and disease progression for individual patients. Full assessment of the strengths and weaknesses of new diagnostic tests and evaluation of when they are best used will be key to proper interpretation of the results, permitting tailored referrals and treatments. Treatment options for individual patients are increasing, including the regeneration of lost bone and connective tissue. Restorative materials are continuously improving, resulting in safe, effective, and aesthetic restorations. The growing field of biomimetics should continue to revolutionize oral health and oral health care. Development of biocompatible restorative and implant materials will continue, as well as development of new biologically engineered substitutes for lost bone, connective tissue, and diseased articular disks, to name several possibilities. Harnessing other basic science knowledge will enable the development of new therapies such as genetically engineered growth factors. Improved understanding of the genetic risk factors, limitation of exposures to teratogens, and attention to diet may markedly diminish the occurrence of congenital anomalies such as cleft lip and palate.

Science is continuing to reveal the intricacies and complexities of disease etiology and pathogenesis. In turn, the classification and diagnosis of diseases and conditions will improve and lead to tailored treatment options. The recent efforts to understand and define early childhood caries are an example of this evolutionary process (Ismail et al. 1999). This example further demonstrates that disease definitions are important for population-based research (Drury et al. 1999, Kaste et al. 1999).

One area critical to the ability of dentists to adopt new treatment modalities or diagnostic techniques is the development of diagnostic codes. In contrast to medicine, these diagnostic codes currently have no impact on reimbursement. However, the development and introduction of such codes are essential for the conduct of needed outcomes research, and their widespread use is necessary for practice-based research. Such codes permit the documentation of preexisting conditions, monitoring of disease progression, and provision of surveillance data in public health programs. A pilot study in a Canadian public health program has proposed and implemented a set of diagnostic codes (Leake et al. 1999). The American Dental Association has undertaken the development of a comprehensive set of diagnostic codes, expected to be released in the near future.

back to top

Broadening the Base for the Provision of Oral Health Care

Further biologic, scientific, and technological advances and changes in the organization of health care delivery will continue to alter future professional and individual health care practices (see Chapters 9 and 11). The increased knowledge of risk factors, the importance of monitoring disease progression and treatment effects, and the ability to diagnose conditions and intervene earlier will necessitate increased involvement of all health professionals in oral health care and may reflect changes in care provision and referral patterns. Management of conditions such as oral and pharyngeal cancers, cleft lip/palate, and chronic pain requires multidisciplinary teams. The promotion of oral health and the prevention of oral disease are at a turning point. A systematic approach to integrate the scientific findings into evidence-based assessments will provide clearer guidance to all health care professions and the public. To capitalize on the rapidly emerging science base, the active participation of a full range of health care providers and individuals and the community is needed.

back to top


  • Achieving and maintaining oral health require individual action, complemented by professional care as well as community-based activities.

  • Individuals can take actions, for themselves and for persons under their care, to prevent disease and maintain health. Primary prevention of many oral, dental, and craniofacial diseases and conditions is possible with appropriate diet, nutrition, oral hygiene, and health-promoting behaviors, including the appropriate use of professional services. Individuals should use a fluoride dentrifice daily to help prevent dental caries and should brush and floss daily to prevent gingivitis.

  • All primary care providers can contribute to improved oral and craniofacial health. Interdisciplinary care is needed to manage the oral health–general health interface. Dentists, as primary care providers, are uniquely positioned to play an expanded role in the detection, early recognition, and management of a wide range of complex oral and general diseases and conditions.

  • Nonsurgical interventions are available to reverse disease progression and to manage oral diseases as infections.

  • New knowledge and the development of molecular and genetically based tests will facilitate risk assessment and management and improve the ability of health care providers to customize treatment.

  • Health care providers can successfully deliver tobacco cessation and other health promotion programs in their offices, contributing to both overall health and oral health.

  • Biocompatible rehabilitative materials and biologically engineered tissues are being developed and will greatly enhance the treatment options available to providers and their patients.

back to top




Ainamo J, Barmes D, Beagrie G, Cutress T, Martin J, Sardo-Infirri J. Development of the World Health Organization (WHO) community periodontal index of treatment needs (CPITN). Int Dent J 1982;32(3):281-91.

Albrektsson T. A multicenter report on osseointegrated oral implants. J Prosthet Dent 1988;60:75-84.

Albrektsson T, Dahl E, Enbom L, Engevall S, Engquist B, Eriksson AR, Feldmann G, Freiberg N, Glantz PO, Kjellman O, et al. Osseointegrated oral implants: a Swedish multicenter study of 8139 consecutively inserted Nobelpharma implants. J Periodontol 1988;59:287-96.

American Academy of Periodontology (AAP). World Workshop on Clinical Periodontitis Consensus Report. Ann Periodontol 1996;1:926-32.

American Dental Association (ADA). A guide to the use of fluorides for the prevention of dental caries. J Am Dent Assoc 1986;113:505-65.

American Dental Association (ADA). New fluoridation guidelines proposed. J Am Dent Assoc 1994;125:136.

American Dental Association (ADA), Council on Access, Prevention and Interprofessional Relations. Caries diagnosis and risk assessment. A review of preventive strategies and management. J Am Dent Assoc 1995;126:15-245.

Anderson MH, Bales DJ, Omnell KA. Modern management of dental caries: the cutting edge is not the dental bur. J Am Dent Assoc 1993;124:37-44.

Angmar-Månsson B, Al-Khateeb S, Tranaeus S. Intraoral use of quantitative light-induced fluorescence for caries detection. In: Stookey GK, editor. Early detection of dental caries. Indianapolis: Indiana University School of Dentistry; 1996. p. 105-18.

Armitage GC. Periodontal diseases: diagnosis. Ann Periodontol 1996;1:37-215.

Armitage GC, Jeffcoat MK, Chadwick DE, Taggart EJ Jr, Numabe Y, Landis JR, Weaver SL, Sharp TJ. Longitudinal evaluation of elastase as a marker for the progression of periodontitis. J Periodontol 1994;65:120-8.

Axelsson P, Lindhe J, Nystrom B. On the prevention of caries and periodontal disease. Results of a 15-year longitudinal study in adults. J Clin Periodontol 1991;18(3):182-9.

Bader JD, Shugars D. Variation in dentists' clinical decisions. J Public Health Dent 1995;55:181-8.

Bawden JW, editor. Changing patterns of fluoride intake. Proceedings of the workshop. J Dent Res 1992;71:1212-27.

Beck J. Identification of risk factors. In: Bader JD, editor. Risk assessment in dentistry: proceedings of a conference, 1989 June 2-39: Chapel Hill, NC. Chapel Hill: University of North Carolina School of Dentistry; 1990.

Benn DK, Watson TF. Correlation between film position, bitewing shadows, clinical pitfalls and the histologic size of approximal lesions. Quintessence Int 1989:20:131-41.

Berkowitz RJ, Jordan HV, White G. The early establishment of Streptococcus mutans in the mouths of infants. Arch Oral Biol 1975;30:171-4.

Bero LA, Grilli R, Grimshaw JM, Harvey E, Oxman AD, Thomson MA. Closing the gap between research and practice: an overview of systematic reviews of interventions to promote the implementation of research findings. The Cochrane effective practice and organization of care review group. BMJ 1998 Aug 15;317(7156):465-8.

Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, Bernstein L, Schoenberg JB, Stemhagen A, Fraumeni JF. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 1988;48:3282-7.

Boice JD, et al. Multiple primary cancers in Connecticut and Denmark. Washington: US GPO; 1985.

Bricker SL, Langlais RP, Miller CS. Oral diagnosis, oral medicine, and treatment planning. Philadelphia: Lea and Febiger; 1994.

Burt BA, Ismail AI. Diet, nutrition, and food cariogenicity. J Dent Res 1986;65:1475-84.

Buser D, Schroeder A, Sutter F, Lang N. The new concept of ITI hollow-cylinder and hollow-screw implants: part 2. Clinical aspects, indications, and early clinical results. Int J Oral Maxillofac Implants 1988;3:173-81.

Buser D, Weber HP, Bragger U, Balsiger C. Tissue integration of one-stage ITI implants: 3-year results of a longitudinal study with hollow-cylinder and hollow-screw implants. Int J Oral Maxillofac Implants 1991;6:405-12.

Califano J, van der Riet P, Westra W, Nawroz H, Clayman G, Piantadosi S, Corio R, Lee D, Greenberg B, Sidransky D, et al. Genetic progression model for head and neck cancer: implications for field cancerization. Cancer Res 1996;56(11):2488-92.

Caufield PW, Cutter GR, Dasanayake AP. Initial acquisition of mutans streptococci infections in infants: evidence for a discrete window of infectivity. J Dent Res 1993;72:37-45.

Cavanaugh PF, Meredith MP, Buchanan W, Doyle MJ, Reddy MS, Jeffcoat MK. Coordinate production of PGE2 and IL-1 in the gingival crevicular fluid of adults with periodontitis: its relationship to alveolar bone loss and disruption by twice daily treatment with ketorolac tromethamine oral rinse. J Periodontal Res 1998;33:75-82.

Centers for Disease Control and Prevention (CDC). Recommendations for using fluoride to prevent and control dental caries in the United States. In press.

Chambers DA, Imrey PB, Cohen RL, Crawford JM, Alves ME, McSwiggin TA. A longitudinal study of aspartate aminotransferase in human gingival crevicular fluid. J Periodontal Res 1991;26:65-74.

Clark GT, Delcanho RE, Goulet JP. The utility and validity of current diagnostic procedures for defining temporomandibular disorder patients. Adv Dent Res 1993;7:97-112.

Clarkson JE, Ellwood RP, Chandler RE. A comprehensive summary of fluoride dentifrice caries clinical trials. Am J Dent 1993 Sep;6(Spec No):S59-106.

Cobb CM. Non-surgical pocket therapy: mechanical. Ann Periodontol 1996;1:443-90.

Cochran D. Implant therapy I. Ann Periodontol 1996;1:707-90.

Cohen SJ, Stookey GK, Katz BP, Drook CA, Christen AG. Helping smokers quit: a randomized controlled trial with private practice dentists. J Am Dent Assoc 1989;118:41-5.

Cutress TW, Powell RN, Kilisimasi S, Tomiki S, Holborow D. A 3-year community-based periodontal disease prevention programme for adults in a developing nation. Int Dent J 1991;41(6):323-34.

de Josselin de Jong E, Hall AF, van der Veen MH. Quantitative light-induced fluorescence for caries detection. In: Stookey GK, editor. Early detection of dental caries. Indianapolis: Indiana University School of Dentistry; 1996. p. 91-103.

Douglass CW. Risk assessment in dentistry. J Dent Educ 1998;62:756-61.

Drisko CH. Non-surgical pocket therapy: pharmacotherapeutics. Ann Periodontol 1996;1:491-566.

Drury TF, Horowitz AM, Ismail AI, Maertens MP, Rozier RG, Selwitz RH. Diagnosing and reporting early childhood caries for research purposes. A report of a workshop sponsored by the National Institute of Dental and Craniofacial Research, the Health Resources and Services Administration, and the Health Care Financing Administration. J Public Health Dent 1999 Summer;59(3):192-7.

Dworkin SF. Perspectives on the interaction of biological, psychological and social factors in TMD. J Am Dent Assoc 1994;125:856-63.

Edelstein BL. The medical management of dental caries. J Am Dent Assoc 1994;125:31s-39s.

Ellwood RP, Davies R, Worthington HV. Evaluation of a dental subtraction radiography system. J Periodontal Res 1997;32(2):241-8.

Evidence-Based Medicine Working Group. Evidence-based medicine: a new approach to teaching the practice of medicine. JAMA 1992;268:2420-5.

Featherstone JD. Clinical implications of early caries detection: new strategies for caries prevention. In: Stookey GK, editor. Early detection of dental caries. Indianapolis: Indiana University School of Dentistry; 1996. p. 285-93.

Featherstone JD, Barrett-Vespone NA, Fried D, Kantorowitz Z, Seka W. CO2 laser inhibition of artificial caries-like lesion progression in dental enamel. J Dent Res 1998;77:1397-403.

Field EA, Field JK, Martin MV. Does Candida have a role in oral epithelial neoplasia? J Med Vet Mycol 1989;27:277-94.

Field M, Lohr K, editors. Guidelines for clinical practice: from development to use. Washington: National Academy Press; 1992.

Fiore MC. Smoking cessation: a systems approach. Clinical practice guideline, no. 18. Rockville (MD): Agency for Health Care Policy and Research; 1997. AHCPR Pub. no. 97-0698. Available from:

Flaitz CM, Hicks MJ. Molecular piracy: the viral link to carcinogenesis. Oral Oncol 1998;34:448-53.

Fletcher SW, Fletcher RH. Development of clinical guidelines. Lancet 1998;12;352(9144):1876.

Food and Drug Administration (FDA). The selection of patients for x-ray examination: dental radiographic examinations. Rockville (MD): Food and Drug Administration; 1987. DHHS Pub. no. 88-8273.

Fritz ME. Implant therapy II. Ann Periodontol 1996;1:796-815.

Garrett S. Periodontal regeneration around natural teeth. Ann Periodontol 1996;1:621-66.

Geiger AM, Gorelick L, Gwinnett AJ, Benson BJ. Reducing white spot lesions in orthodontic populations with fluoride rinsing. Am J Orthod Dentofac Orthop 1992;101(5):403-7.

Geivelis M, Turner DW, Pederson ED, Lamberts BL. Measurements of interleukin-6 in gingival crevicular fluid from adults with destructive periodontal disease. J Periodontol 1993;64:980-3.

Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996 Oct;67(10 Suppl):1041-9.

Genco RJ. Risk factors for periodontal disease. In: Rose LF, Genco RJ, Cohen DW, Mealey BL, editors. Periodontal medicine. Hamilton (Ontario): B.C. Decker Inc.; 2000.

Genco RJ, Newman MG, editors. Consensus report on prevention. Proceedings of the 1996 World Workshop in Periodontics. Ann Periodontol 1996;1:250-5.

Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress, and inadequate coping behaviors to periodontal disease. J Periodontol 1999;70:711-23.

Goodson JM, Cugini MA, Kent RL, Armitage GA, Cobb CM, Fine D, Fritz ME, Green E, Imoberdorf MJ, Killoy WJ, et al. Multicenter evaluation of tetracycline fiber therapy: II. Clinical response. J Periodontal Res 1991;26:371-9.

Graves RC, Disney JA, Stamm JW. Comparative effectiveness of flossing and brushing in reducing interproximal bleeding. J Periodontol 1989;60(5)243-7.

Gröndahl HG. Radiographic assessment of caries and caries progression. In: Anusavice KJ, editor. Quality evaluation of dental restoration: criteria for placement and replacement. Chicago: Quintessence Publishing Co.; 1989. p. 151-67.

Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: a two-way relationship. Ann Periodontol 1998 Jul;3(1):51-61.

Grossi SG, Skrepcinski FB, DeCoro T, Zambon JJ, Cummin SD, Genco RJ. Response to periodontal therapy in diabetics and smokers. J Periodontol 1996;67:1094-102.

Guckes AD, Roberts MW, McCarthy GR. Pattern of permanent teeth present in individuals with ectodermal dysplasia and severe hypodontia suggests treatment with dental implants. Pediatr Dent 1998;20:278-80.

Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol 2000 1994;5:78-111.

Haffajee AD, Socransky SS, Goodson JM. Clinical parameters as predictors of destructive periodontal disease activity. J Clin Periodontol 1983;10:257-65.

Halazonetis TD, Haffajee AD, Socransky SS. Relationship of clinical parameters to attachment loss in subsets of subjects with destructive periodontal diseases. J Clin Periodontol 1989;16:563-8.

Hancock EB. Prevention. Ann Periodontol 1996;1:223-49.

Head JA. A study of saliva and its action on tooth enamel in reference to its hardening and softening. JAMA 1912;59:2118-22.

Hillman JD, Brooks TA, Michalek SM, Harmon CC, Snoep JL, van Der Weijden CC. Construction and characterization of an effector strain of Streptococcus mutans for replacement therapy of dental caries. Infect Immun 2000;68:543-9.

Ismail AI. Clinical diagnosis of precavitated carious lesions. Community Dent Oral Epidemiol 1997;25:13-23.

Ismail AI, Bader JD, Kamerow DB. Systematic reviews and the practice of evidence-based dentistry: professional and policy implications. J Am Coll Dent 1999;66:5-12.

Jeffcoat MK. Imaging techniques for the periodontium. In: Wilson TG, Kornman K, Newman MG, editors. Advances in periodontics. Chicago: Quintessence; 1992.

Jeffcoat MK, Wang IC, Reddy MS. Radiographic diagnosis in periodontitis. Periodontol 2000 1995;7:54-68.

Jeffcoat MK, Reddy MS, Magnusson I, Johnson B, Meredith MP, Cavanaugh PF Jr, Gerlach RW. Efficacy of quantitative digital subtraction radiography using radiographs exposed in a multicenter trial. J Periodontal Res 1996;31(3):157-60.

Jeffcoat MK, McGuire M, Newman MG. Evidence-based periodontal treatment: highlights from the 1996 World Workshop in Periodontics. J Am Dent Assoc 1997;128:713-24.

Jeffcoat MK, Bray K, Ciancio SG, Dentino AR, Fine DH, Gordon JM, Gunsolley JC, Killoy WJ, Lowenguth RA, Magnusson NI, et al. Adjunctive use of a subgingival controlled-release chlorhexidine chip reduces probing pocket depth and improves attachment level compared with scaling and root planing alone. J Periodontol 1998 Sep;69(9):989-97.

Johnson NW. Orofacial neoplasms: global epidemiology, risk factors and recommendations for research. Int Dent J 1991;41(6):365-75.

Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: I. Response to 4 therapeutic modalities. J Periodontol 1996;67:93-102.

Kantorowitz Z, Featherstone JD, Fried D. Caries prevention by CO2 laser treatment: dependency on the number of pulses used. J Am Dent Assoc 1998;129:585-91.

Kaste LM, Drury TF, Horowitz AM, Beltran E. An evaluation of NHANES III estimates of early childhood caries. J Public Health Dent 1999;59:198-200.

Katz S. The use of fluoride and chlorhexidine for the prevention of radiation caries. J Am Dent Assoc 1982;104:164-70.

Kearns G, Sharma A, Perrott D, Schmidt B, Kaban L, Vargerik K. Placement of endosseous implants in children and adolescents with hereditary ectodermal dysplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88(1):5-10.

Ketley CE, Holt RD. Visual and radiographic diagnosis of occlusal caries in first permanent molars and in second primary molars. Br Dent J 1993;174:364-70.

Kidd EA. Caries diagnosis within restored teeth. Adv Den Res 1990 Jun;4:10-3.

Knowles JW, Burgett FG, Nissle RK, Shick RA, Morrison EC, Ramfjord SP. Results of periodontal treatment related to pocket depth and attachment level. Eight years. J Periodontol 1979;50:225-33.

Kohler B, Bratthall D. Intra-familial levels of Streptococcus mutans and some aspects of the bacterial transmission. Scand J Dent Res 1978;86:35-42.

Kornman KS, Crane A, Wang HY, di Giovine FS, Newman MG, Pirk FW, Wilson TJ Jr, Higginbottom FL, Duff GW. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol 1997;24(1):72-7.

Koulourides T, Ceuto H, Pigman W. Rehardening of softened enamel surfaces of human teeth by solutions of calcium phosphates. Nature 1961;189:226-7.

Lamster IB, Smith QT, Celenti RS, Singer RE, Grbic JT. Development of a risk profile for periodontal disease: microbial and host response factors. J Periodontol 1994;65:511-20.

Lamster IB, Holmes LG, Gross KB, Oshrain RL, Cohen DW, Rose LF, Peters LM, Pope MR. The relationship of beta-glucuronidase activity in crevicular fluid to probing attachment loss in patients with adult periodontitis. Findings from a multicenter study. J Clin Periodontol 1995;22(1):36-44.

Lang NP, Joss A, Orsanic T, Gusberti FA, Siegrist BE. Bleeding on probing. A predictor for the progression of periodontal disease? J Clin Periodontol 1986;13:590-6.

Lang WP, Farghaly MM, Ronis DL. The relation of preventive dental behaviors to periodontal health status. J Clin Periodontol 1994;21(3):194-8.

Larsen MJ, Fejerskov O. Chemical and structural challenges in remineralization of dental enamel lesions. Scand J Dent Res 1987;97:285-96.

Leake JL, Main PA, Sabbah W. A system of diagnostic codes for dental health care. J Public Health Dent 1999;59(3):162-70.

Lee W, Aitken S, Sodek J, McCulloch CA. Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis. J Periodontal Res 1995 Jan;30(1):23-33.

Levy SM. Review of the fluoride exposures and ingestion. Community Dent Oral Epidemiol 1994 Jun;22(3):173-80.

Lewis DW, Ismail AI. Periodic health examination, 1995 update: 2. Prevention of dental caries. Canadian Task Force on the Periodic Health Examination. Can Med Assoc J 1995;152:836-46.

Li Y, Caufield PW. The fidelity of initial acquisition of mutans streptococci by infants from their mothers. J Dent Res 1995 Feb;74(2):681-5.

Linton JL. Quantitative measurements of remineralization of incipient caries. Am J Orthod Dentofac Orthop 1996;110:590-7.

Lippman SM, Benner SE, Hong WK. Chemoprevention. Cancer 1993;984-90.

Löe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533-51.

Loesche WJ. The identification of bacteria associated with periodontal disease and dental caries by enzymatic methods. Oral Microbiol Immunol 1986;1:65-70.

Loesche WJ, Giordona J, Hujoel PP. The utility of the BANA test for monitoring anaerobic infections due to spirochetes (Treponema denticola) in periodontal disease. J Dent Res 1990 Oct;69(10):1696-702.

Lussi A. Comparison of different methods for the diagnosis of fissure caries without cavitation. Caries Res 1993;27:409-16.

Lussi A, Firestone A, Schoenberg V, Hotz P, Stich H. In vivo diagnosis of fissure caries using a new electrical resistance monitor. Caries Res 1995;29:81-7.

Ma JK, Hikmat BY, Wycoff K, Vine ND, Chargelegue D, Yu L, Hein MB, Lehner T. Characterization of a recombinant plant monoclonal secretory antibody and preventive immunotherapy in humans. Nat Med 1998 May;4(5):601-6.

Mandel ID. Calculus update: prevalence, pathogenicity and prevention. J Am Dent Assoc 1995 May;126(5):573-80.

Masada MP, Persson R, Kenney JS, Lee SW, Page RC, Allison AC. Measurement of interleukin-1 alpha and -1 beta in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. J Periodontal Res 1990;25:156-63.

Matsuda Y, Byrd V, et al. A comparison of the accuracy of a direct digital radiography and conventional firm based subtraction system in detecting bony change. In: Farman AG, editor. Advances in maxillofacial imaging: IADMFR/CMI'97 selected proceedings of the 11th Congress of the International Association of Dentomaxillofacial Radiology and the 3rd International Congress and Exposition on Computed Maxillofacial Imaging, Louisville, KY, 1977 Jun 21-27. New York: Elsevier; 1997. p. 56-66.

McLaughlin JK, Gridley G, Block G, Winn DM, Preston-Martin S, Schoenberg JB, Greenberg RS, Stemhagen A, Austin DF, Ershow AG, et al. Dietary factors in oral and pharyngeal cancer. J Natl Cancer Inst 1988;80(15):1237-43.

Mealey BL. Periodontal implications: medically compromised patients. Ann Periodontol 1996;1:256-321.

Mellonig JT. Donor selection, testing, and inactivation of the HIV virus in freeze-dried bone allografts. Pract Periodontics Aesthetic Dent 1995;7(6):13-22.

Mertz-Fairhurst EJ, Curtis JS, Ergle JW, Rueggeberg FA, Adair SM. Ultraconservative and cariostatic sealed restorations: results at year 10. J Am Dent Assoc 1998;129:55-66.

Meyerowitz C, Featherstone JD, Billings RJ. Use of an intra-oral model to evaluate 0.05% sodium fluoride mouthrinse in radiation-induced hyposalivation. J Dent Res 1991;70(5):894-8.

Mjör IA. Frequency of secondary caries at various anatomical locations. Oper Dent 1985;10:88-92.

Mohl ND, Lund JP, Widmer CG, McCall WD Jr. Devices for the diagnosis and treatment of temporomandibular disorders. J Prosthet Dent 1990;63:332-6.

Moncla BJ, Strockbine L, Braham P, Karlinsey J, Roberts MC. The use of whole-cell DNA probes for the identification of Bacteroides intermedius isolates in a dot blot assay. J Dent Res 1988;67:1267-70.

Moore WE. Microbiology of periodontal disease. J Periodontal Res 1987;22:335-41.

Moss SJ, editor. Fluorides: an update for dental practice. The American Academy of Pedodontics. New York: Medcom; 1976.

Mount GJ, Hume WR. A revised classification of carious lesions by site and size. Quintessence Int 1997;28:301-3.

Mount GJ, Hume WR. Preservation and restoration of tooth structure. London: Mosby; 1998.

Murphy GP, Lawrence W Jr, Lenhard RE Jr, editors. American Cancer Society textbook of clinical oncology. Atlanta: American Cancer Society; 1995. p. 180.

National Cancer Institute (NCI). Cigars. Health effects and trends. Bethesda (MD): National Institutes of Health; 1998. p. 232. NIH Pub no. 98-4302.

National Institutes of Health (NIH). Technology Assessment Conference Statement, 1996 Apr 29-May 1. Management of temporomandibular disorders. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, Office of Medical Applications of Research; 1996. p. 1-31.

Newbrun E, Leverett D. Risk assessment dental caries working group summary statement. In: Bader JD, editor. Risk assessment in dentistry: proceedings of a conference, June 2-3, 1989, Chapel Hill, North Carolina. Chapel Hill: University of North Carolina School of Dentistry; 1990. p. 304.

Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ. Calcium and risk for periodontal disease. Periodontol 2000;70(7):in press.

Ockene JK, Kristellar J, Goldberg R. Increasing the efficacy of physician-delivered smoking interventions: a randomized clinical trial. J Gen Intern Med 1991;6:1-8.

Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. J Periodontal Res 1986;21:101-12.

Ohtoshi T, Yamauchi K, Tadokoro K, Miyachi S, Suzuki S, Miyamoto T, Muranaka M. IgE antibody-mediated shock reaction caused by topical application of chlorhexidine. Clin Allergy 1986;16:155-61.

Okamoto H, Yoneyama T, Lindhe J, Haffajee A, Socransky S. Methods of evaluating periodontal disease data in epidemiological research. J Clin Periodontol 1988;15:430-9.

Okano M, Nomura M, Hata S, Okada N, Sato K, Kitano Y, Tashiro M, Yoshimoto Y, Hama R, Aoki T. Anaphylactic symptoms due to chlorhexidine gluconate. Arch Dermatol 1989;125(1):50-2.

Page RC. Periodontal diseases: a new paradigm. J Dent Educ 1998;62:812-21.

Page RC, Beck JD. Risk assessment for periodontal diseases. Int Dent J 1997;47:61-87.

Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000 1997;14:9-11.

Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 1976 Mar;34(3):235-49.

Palcanis KG. Surgical pocket therapy. Ann Periodontol 1996;1:589-617.

Palcanis KG, Larjava IK, Wells BR, Suggs KA, Landis JR, Chadwick DE, Jeffcoat MK. Elastase as an indicator of periodontal disease progression. J Periodontol 1992;63:237-42.

Papapanou PN. Risk assessments in the diagnosis and treatment of periodontal diseases. J Dent Educ 1998;62:822-39.

Patterson IC, Eveson JW, Prime SS. Molecular changes in oral cancer may reflect aetiology and ethnic origin. Eur J Cancer 1996;32B:150-3.

Penning C, van Amerongen JP, Seef RE, ten Cate JM. Validity of probing for fissure caries diagnosis. Caries Res 1992;26:445-9.

Persson GR, Page RC. Diagnostic characteristics of crevicular fluid aspartate aminotransferase (AST) levels associated with periodontal disease activity. J Clin Periodontol 1992;19:43-8.

Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Comparison of surgical and non-surgical treatment of periodontal disease. J Clin Periodontol 1983;10:524-41.

Pitts NB. Risk assessment and caries prediction. J Dent Educ 1998;62:762-70.

Pitts NB, Longbottom C. Preventive care advised (PCA)/Operative care advised (OCA)—categorising caries by the management option. Community Dent Oral Epidemiol 1995;23:55-9.

Pogoda JM, Preston-Martin S. Solar radiation, lip protection, and lip cancer in Los Angeles County women (California, United States). Cancer Causes Control 1996;7:458-63.

Powell LV. Caries prediction: a review of the literature. Community Dent Oral Epidemiol 1998;26:361-71.

Qvist V, Laurberg L, Poulsen A, Teglers PT. Longevity and cariostatic effects of everyday conventional glass-ionomer and amalgam restorations in primary teeth: three year results. J Dent Res 1997;76(7):1387-96.

Ramfjord SP, Caffesse RG, Morrison EC, Hill RW, Kerry GJ, Appleberry EA, Nissle RP, Stults DL. Four modalities of periodontal treatment compared over 5 years. J Clin Periodontol 1987;14(8):445-52.

Ranney RR. Classification of periodontal disease. Periodontol 2000 1993;2:13-25.

Rao VM. Imaging of the temporomandibular joint. Semin Ultrasound CT MR 1995;16(6):513-26.

Rao VM, Farole A, Karasick D. Temporomandibular joint dysfunction; correlation of MR imaging, arthrography and arthroscopy. Radiology 1990;174:663-7.

Reddi H. Bone morphogenetic proteins. Adv Dent Res 1995:9(3 Suppl):13.

Ries LAG, Kosary CL, Hankey BF, Miller BA, Edwards BK, editors. SEER Cancer Statistics Review, 1973-1996. Bethesda (MD): National Cancer Institute; 1999.

Ronis DL, Lang WP, Farghaly MM, Passow E. Tooth brushing, flossing and preventive dental visits by Detroit-area residents in relation to demographic and socioeconomic factors. J Public Health Dent 1993 Summer;53(3):138-45.

Rose LF, Steinberg BJ. Clinical history and laboratory tests. In: Rose LF, Genco RJ, Cohen DW, Mealey BL, editors. Periodontal medicine. Hamilton (Ontario): B.C. Decker Inc.; 2000.

Rossomando EF, Kennedy JE, Hadjimichael J. Tumour necrosis factor alpha in gingival crevicular fluid as a possible indicator of periodontal disease in humans. Arch Oral Biol 1990;35:431-4.

Russell MW, Hajishengallis G, Childers NK, Michalek SM. Secretory immunity in defense against cariogenic mutans streptococci. Caries Res 1995;33:4-15.

Sackett DL, Rosenberg WM, Muir Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn't. BMJ 1996;312:71-2.

Savitt ED, Strzempko MN, Vaccaro KK, Peros WJ, French CK. Comparison of cultural methods and DNA probe analyses for detection of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, and Bacteroides intermedius in subgingival plaque samples. J Periodontol 1988;59:431-8.

Savitt ED, Keville MW, Peros WJ. DNA probes in the diagnosis of periodontal microorganisms. Arch Oral Biol 1990;35(Suppl):153S-9S.

Schaeken MJ, Keltjens HM, van der Hoeven JS. Effects of fluoride and chlorhexidine on the microflora of dental root surfaces and progression of root-surface caries. J Dent Res 1991;70(2):150-3.

Schroeder HE, Munzel-Pedrazzoli S, Page R. Correlated morphometric and biochemical analysis of gingival tissue in early chronic gingivitis in man. Arch Oral Biol 1973;18:899-923.

Schwartz SM, Daling JR, Doody DR, Wipf GC, Carter JJ, Madeleine MM, Mao EJ, Fitzgibbons ED, Huang S, Beckmann AM, et al. Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection. J Natl Cancer Inst 1998;90:1626-36.

Sciubba JJ. Improving detection of precancerous and cancerous oral lesions: computer-assisted analysis of the oral brush biopsy. J Am Dent Assoc 1999;130:1445-58.

Scully C. Oral precancer: preventive and medical approaches to management. Oral Oncol Euro J Cancer 1995;31B:16-26.

Shah JP, Lydiatt W. Treatment of cancer of the head and neck. CA Cancer J Clin 1995;45:352-68.

Shin DM, Lee JS, Lippman SM, Lee JJ, Tu ZN, Choi G, Heyne K, Shin HJ, Ro JY, Goepfert H, et al. P53 expressions: predicting recurrence and second primary tumors in head and neck squamous cell carcinoma. J Natl Cancer Inst 1996;88(8):519-29.

Shugars D, Bader J. Practice parameters in dentistry: where do we stand? J Am Dent Assoc 1995;126:1134-43.

Sidransky D. Nucleic acid-based methods for the detection of cancer. Science 1997;278:1054-9.

Silverman S Jr. Oral cancer. Atlanta: American Cancer Society; 1990.

Silverstone LM, Wefel JS, Zimmerman BF, Clarkson BH, Featherstone MJ. Remineralization of natural and artificial lesions in human dental enamel in vitro. Caries Res 1981;15:138-57.

Socransky SS, Haffajee AD. The bacterial etiology of destructive periodontal disease: current concepts. J Periodontol 1992;63:322-31.

Spiekermann H, Jansen V, Richter EJ. A 10-year follow-up study of IMZ and TPS implants in the edentulous mandible using bar-retained overdentures. Int J Oral Maxillofac Implants 1995;10:231-43.

Spitz MR, Fueger JJ, Goepfert H, Hong WK, Newell GR. Squamous cell carcinoma of the upper digestive tract. A case comparison analysis. Cancer 1988;61:203-8.

Stevens VJ, Severson H, Lichtenstein E. Little SJ, Leben J. Making the most of a teachable moment; a smokeless-tobacco cessation intervention in the dental office. Am J Public Health 1995;85(2):231-5.

Stookey GK, DePaola PF, Featherstone JD, Fejerskov O, Moller IJ, Rotberg S, Stephen KW, Wefel JS. A critical review of the relative anticaries efficacy of sodium fluoride and sodium monofluorophosphate dentifrices. Caries Res 1993;27(4):337-60.

Sugerman PB, Shillitoe EJ. The high risk human papillomaviruses and oral cancer: evidence for and against a causal relationship. Oral Dis 1997;3:130-47.

Tavender E. The Cochrane collaboration and the oral health review group. Evidence-based dentistry; 1999 Jun.

Tenovuo J, Häkkinen P, Paunio P, Emilson CG. Effects of chlorhexidine-fluoride gel treatments in mothers on the establishment of mutans streptococci in primary teeth and development of dental caries in children. Caries Res 1992;26:275-80.

Thylstrup A, Vinther D, Christiansen J. Treatment time studies during 1 year in a Danish public child dental health service. Caries Res 1995;29:292.

Tolarova MM, Harris J. Reduced recurrence of orofacial clefts after peri-conceptional supplementation with high dose folic acid and multivitamins. Teratology 1995;51:71-8.

Travell J, Simons D. Myofascial pain and dysfunction: the trigger point manual. The upper extremities. Baltimore: Williams and Wilkins; 1983.

Tsai CC, Ho YP, Chen CC. Levels of interleukin-1 and interleukin-8 in gingival crevicular fluids in adult periodontitis. J Periodontol 1995;66:852-9.

Urist MR. Bone formation by autoinduction. Science 1965;150:893-9.

Urist MR, Iwata H. Preservation and biodegradation of the morphogenetic property of bone matrix. J Theor Biol 1973;38:155-67.

U.S. Department of Health and Human Services (USDHHS). Detecting oral cancer: a guide for health care professionals. Washington: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Dental Research; 1998 Jan.

Vokes EE, Athanasiadis I. Chemotherapy for squamous cell carcinoma of head and neck: the future is now. Ann Oncol 1996;7:15-29.

Vokes EE, Weichselbaum RR, Lipman SM. Head and neck cancer. N Engl J Med 1993;328:184-94.

Walsh M, Heckman B, Leggott P, Armitage G, Robertson PB. Comparison of manual and power toothbrushing with and without adjunctive oral irrigation, for controlling plaque and gingivitis. J Clin Periodontol 1989;16(7):419-27.

Werler MM, Louik C, Mitchell AA. Achieving a public health recommendation for preventing neural tube defects with folic acid. Am J Public Health 1999;89:1637-40.

White DJ. Reactivity of fluoride dentifrices with artificial caries; II. Effects on subsurface lesions, F uptake, surface hardening, and remineralization. Caries Res 1988;22:27-36.

Wilson DM, Taylor DW, Gilbert JR, Best JA, Lindsay EA, Willms DG, Singer J. A randomized trial of a family physician intervention for smoking cessation. JAMA 1988;260(11):1570-4.

Winn DM, Blot WJ. Second cancer following cancer of the buccal cavity and pharynx in Connecticut, 1935-82. In: Boice JD, et al. Multiple primary cancers in Connecticut and Denmark. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute; 1985.

Winn DM, Blot WJ, McLaughlin JK, Austin DF, Greenberg RS, Preston-Martin S, Schoenberg JB, Fraumeni JF Jr. Mouthwash use and oral conditions in the risk of oral and pharyngeal cancer. Cancer Res 1991;1(11)3044-7.

Zambon JJ, Bochacki V, Genco RJ. Immunological assays for putative periodontal pathogens. Oral Microbiol Immunol 1986;1:39-44.

Zarb GA. Temporomandibular joint and masticatory muscle disorders. 2nd ed. Copenhagen: Munksgaard; 1994.

Zheng Z-F, et al. Marijuana use and increased risk of squamous cell carcinoma of the head and neck. Cancer Epidemiol Biomark Prev 1999;8:1071-8.

back to top

1 The term prevention, as used in this chapter, includes interventions aimed at reducing the incidence of disease in relatively healthy patients. It includes both health promotion and specific protection to control one or more risk factors. Some strategies, such as the prevention of tobacco use, are applicable to many oral diseases, including oral cancer, oral candidiasis, and periodontal diseases, whereas other strategies are specific, such as the use of dental sealants and fluorides for caries prevention. return to text

2 Sensitivity is a measure of how often the test is positive when applied to patients known to have a particular disease or condition; specificity is a measure of how successful the test is in judging the absence of a disease or condition. return to text

3 Certain systemic tetracyclines, notably doxycycline, are safe and effective in low doses for prevention of bone loss associated with periodontitis. Doxycycline hyclate (20-mg capsule) is approved for twice-a-day use for up to 9 months for this indication. At these low doses, the doxycycline appears to reduce the level of elevated collagenase activity, rather than function as an antimicrobial. return to text

Next: Chapter 9

Share This Page

GooglePlusExternal link – please review our disclaimer

LinkedInExternal link – please review our disclaimer


This page last updated: February 01, 2017