Personal and Provider Approaches to Oral Health Treatment. Prompt UWeatment 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 conser- vative 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 treat- ment 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 para- digm, resulted in a marked reduction of operative procedures in Danish schoolchildren (Thylstrup et al. 1995) and has been proposed as a means to pre- serve tooth structure and maximize appropriate care in the United States (Ismail 1997). New imaging and laser technologies are emerg- ing 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 flu- orescence method and electrical conductance meas- urements, 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-Mansson 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 aes- thetically 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 reha- bilitation 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 den- tal implants. These are used not onty 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 sci- ence with rapidly growing knowledge of the progen- itor cells and molecules that give rise to specific tis- sues 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 infec- tions, and are plaque-related complex diseases like dental caries, presenting as several clinical variants ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 201 Personal and Provider Approaches to Oral Health (see Chapter 3). The mildest form is gingivitis, char- acterized 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 sys- temic 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 environ- mental, acquired, and genetic risk factors specific to a given individual. Figure 8.5 illustrates the patho- genesis of these diseases (Page and Beck 1997). Risk Assessment. Sufficient knowledge of demograph- ic and systemic risk factors and indicators has been acquired to guide clinical decisions in the manage- ment of periodontal diseases (Genco 1996, 2000, Page and Beck 1997, Papapanou 1998). Table 8.7 provides an overview of the strength of the associa- tions 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 mark- er/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 fac- tors that contribute to the likelihood of disease pres- ence, progression, and treatment outcomes. A systematic identification of risk factors, indica- tors, and predictors has been proposed as the first step in diagnosing and managing periodontal dis- eases (Genco 1996, Page and Beck 1997, Papapanou 1998). Clinicians can weigh the known risks for indi- vidual patients and devise treatment plans appropri- FIGURE 8.5 Anew paradigm for the pathobiology of periodontitis Antigens Lipopoly- saccharide virulence factors Environmental and acquired (behavioral) risk factors Antibody Cytokines & prostanoids . Polymorpho- Host Connective Clinical Microbial nuclear immuno- tissue signs of challenge neutrophils inflammatory and bone disease and response metabolism progression Matrix metallo- proteinases Genetic risk factors Source: Page and Kornman 1997. The pathogenesis of human periodontitis: an introduction. Periadontology 2000 1997; 14:9-11. Copyright 1997 by Periodontology 2000. Reprinted by permission of Munksgaard International Publishers Ltd., Copenhagen, Denmark (2000). 202 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health TABLE 8.7 The strength of association of local and systemic factors with destructive periodontal disease Case Report Case-Control Cross-sectional Longitudinal Factor Studies Studies Studies Studies Intervention Studies Specific bacteria P gingivalis Yes Yes " Yes Yes Yes B. forsythus Yes Yes Yes Yes Yes Pintermedia Yes Yes Yes Yes Yes Sex Male Yes NR Yes NR NR Age Yes Yes Yes No (to 7th decade) NR Diabetes mellitus Type 2 Yes Yes Yes Yes Yes (treatment reduces glycosylated hemoglobin) Type 1 Yes Yes Yes NR NR Smoking NR Yes Yes Yes Yes (smokers heal poorly) Osteoporosis Yes Yes Yes NR NR Stress, distress, coping Yes Yes Yes NR NR Polymorphonuclear disorders Yes Yes NR Yes (case series) NR Genetic factors (IL-1 polymorphisms) - NR Yes NR NR NR Dietary calcium NR Yes Yes NR NR Preexisting periodontal disease Yes Yes Yes Yes Yes Note: NR = not reported, or not relevant. Source: Genco 2000. Copyright 1996 by Journal of Periodontology. Reprinted by permission of the Journal of Periodontology (2000). TABLE 8.8 Risk of periodontal disease Strength af Association With Odds Ratio Demographic characteristics Age, 35-44 years alvealar bane loss 2.60 Age, 65-74 years alveolar bone loss 24.08 Risk factors Smoking, light periodontal disease 2.05 alveolar bone loss 1.48 Smoking, heavy periodontal disease 475 alveolar bone loss 7.28 Bacterial risk factors Pear oral hygiene periodontal disease 20.52 P gingivalis periodontal disease 3.60 A. actinomycetemcomitans periodontal disease 2.50 Clinical measurement Bleeding on probing? progression of periodontitis 27 aMeta-analysis (Armitage 1996). Sources: Jeffcoat et al. 1997, Page and Beck 1997. ate 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 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL periodontal health and disease (Genco 1996, 2000, Genco et al. 1999, Papapanou 1998). Most recently, putative genetic markers for sus- ceptibility for oral disease have been studied. In par- ticular, 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 is of interest because the proinflamma- tory 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 Com- munity 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 wd oo } Personal and Provider Approaches to Oral Health 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 (Lée 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 inevi- table progression to destruction (Armitage 1996, Halazonetis et al. 1989, Okamoto et al. 1988). Longi- tudinal studies have also been conducted in patients who participate in maintenance programs. The absence of gingival bleeding, especially at recall vis- its, 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 attach- ment are associated with lack of disease progression. The mere presence of a pocket does not herald pro- gressive 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 pros- thetic reconstructions, as well as a necessary diag- nostic aid in assessing periodontal progression. At least 15 different organisms have been associ- ated with adult periodontitis. The 3 species most and recording (PSR) practice Probing pocket depths _ All patients TABLE 8.9 Strengths and weaknesses of tests and methods used to diagnose periodontal diseases Application Strengths Weaknesses Type of Evidence Periodontal screening —_ All patients in every Cost-effective, quick, easy; detects Does not provide a tooth-by-tooth Epidemiologic studies patients with periodontal disease, Shallow probing depths are associated with lack of future disease progression. assessment for later comparison during maintenance. A full periodontal examination is needed for this purpose. Moderate to deep pockets in single probing depth examination will not distinguish with certainty which teeth will undergo progressive periodontal destruction. Longitudinal studies Gingival inflammation Radiographic evidence of bone loss Microbial/plaque tests Biochemical profiles in gingival crevicular fluid Assessed in all patients At-risk patients as determined by PSR screening or periodontal examination High-risk or refractory patients Not yet determined Absence of inflammation is associated with a lack of future progression. In treated patients, bleeding on probing is associated with an increased risk for pragressive loss of attachment. Absence of bone loss is associated with a lower risk of future progression. Absence of supragingival plaque is associated with lack of disease progression. In compromised or refractory patients, may be useful in determining the presence of pathogens. A number of biochemical markers may identify individuals at risk. Presence of inflammation will not distinguish with certainty which teeth will undergo progressive periodontal destruction. Presence of bone loss ona single radiograph will not distinguish with certainty which teeth will undergo progressive periodontal destruction. At this time, routine testing offers limited benefit in adult periodontitis. At present, there are no specific biochemical profiles that characterize specific periodontal diseases. Longitudinal studies Longitudinal studies Cross-sectional and Longitudinal studies Case reports Cross-sectional and Longitudinal studies 204 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health strongly linked are Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. Actinobacillus actinomycetemcomitans is most strong- ix 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 investi- wators to suspect that periodontitis is a mixed infec- o tion (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 treat- ment programs for special patient populations and as 4 research tool, however, the tests can be very help- ful. Such patients include those refractory to previous therapy, patients with rapidly progressive or early- onset periodontitis, and certain medically compro- mised patients. The traditional method for assessing the subgin- gival 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 anaer- obes, 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 quick- ly and with a high degree of sensitivity and specifici- ty, 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, tell- tale 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 E, (Cavanaugh et al. 1998, Offenbacher et al. 1986), interleukin 1 and inter- leukin 6 (Cavanaugh et al. 1998, Geivelis et al. 1993, Masada et al. 1990, Tsai et al. 1995), tumor necrosis factor (Rossomando et al. 1990), B-glucuronidase (Lamster et al. 1994, 1995), aspartate aminotrans- ferase (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 patients age, oral hygiene, personal habits (e.g., smoking and diet), and a medical history indicating a heightened risk of infection (such as noted with dia- betes or HIV infection) (Hancock 1996, Mealey 1996). Chemical plaque control has become an impor- tant 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 com- bination of essential oils, and stannous fluoride. The magnitude of gingival inflammation reduction was greatest for chlorhexidine. The evidence supporting ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 205 Personal and Provider Approaches to Oral Health 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 treat- ment is to determine whether the disease is active in order to prevent further tissue loss. This entails pro- fessional 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 docu- mented for individuals who smoke and those who are diabetic and may be important for other risk fac- tors such as stress (Genco et al. 1999) and low dietary calcium (Nishida et al. in press). Several stud- ies have shown that treatment of periodontal disease in smokers is not as successful as in nonsmokers (Grossi et al. 1996). Thus, the management of smok- ing as a risk factor will contribute to the success of periodontal therapy. Furthermore, it appears that treatment of diabetic patients with periodontal dis- ease may require more intense therapy since several studies have shown that antibiotic therapy is suc- cessful 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 peri- odontal pocket and the tooth root surface is smoothed over. The effectiveness of scaling and root planing has been demonstrated repeatedly in longi- tudinal, cohort, and randomized clinical trials and was reviewed by Cobb (1996). Demonstrated bene- fits include decreased gingival inflammation, decreased probing depth, and facilitation of mainte- nance of clinical attachment level. The evidence indi- cates that similar results may be obtained with ultra- sonic and sonic instruments as with manual instru- ments. Regardless of the methods used, meticulous attention to detail is required to achieve optimal results (Cobb 1996). TABLE 8.10 Periodontal diseases: mechanical therapy and chemotherapeutics Category of Treatment Treatment Professional mechanical therapy—used in the treatment of gingivitis and periodontitis Scaling and root planing with Manual instrument Ultrasonic and sonic scaling and used as an adjunct to brushing —_ gingivitis Sustained release anti- intrapocket resorbable or non- Strengths Decreases gingival inflammation Requires attention to detail by 40 to 60 percent Decreases probing depth Facilitates gain in clinical attachment level Results are similar to manual Significant reductions in gingival No clear evidence that there is root planing scaling and root planing Chemical plaque control == Chlorhexidine with mouthrinses and Triclosan co-polymer or triclosan inflammation dentifrices zinc-citrate Essential oils Stannous fluoride Irrigation Supra- and subgingival irrigation Aids in the reduction of When used as an adjunct to Weaknesses Type of Evidence Numerous longitudinal, cohort, and randomized clinical trials Longitudinal, cohort, and randomized clinical trials Randomized double-blind a substantial long-term clinical trials benefit for periodontitis except to control co-existing inflammation Randomized double-blind clinical trials No clear evidence that there is a substantial long-term benefit for periodontitis Few reported side effects Randomized double-blind microbials resorbable delivery systems scaling and root planing, gains in include transient discomfort, clinical trials containing a tetracycline clinical attachment level and erythema, recession, allergy, antibiotic decreases in probing depth and —_ and rarely candidiasis bleeding Systemic antibiotics Tetracyclines, metronidazole, May be useful to treat aggressive Not indicated for gingivitis Assessment of risk-benefit spiromycin, clindamycin, and destructive periodontitis Not indicated for most adult ratio combinations such as periodontitis patients Randomized double-blind metronidazole and amoxicillin clinical trials Randomized double-blind clinical trials, longitudinal assessment of patients 206 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health 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 treat- ment 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 dis- ease progression. Many surgical techniques are avail- able. Extensive randomized clinical trials and longi- tudinal 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, how- ever, is that procedures designed to reduce probing depth may increase gum recession, exposing the root and possibly compromising aesthetics. Thus, selec- tion 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, 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 indi- cates that the agents do not offer sufficient benefit to overcome risks of either drug sensitivity or the emer- gence 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 sys- temic 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 incorporat- ed into either resorbable and nonresorbable inter- pocket delivery systems have been studied in ran- domized, 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 control, and enhances width. TABLE 8.11 Periodontal disease: selected surgical procedures Category and Goal Procedures Strengths Weaknesses Type of Evidence Pocket therapy— Modified Widman Flap to All procedures decrease pocket depth. Procedures designed to Randomized clinical trials provides access to root provide access to roots and With the exception of gingivectomy, all reduce probing depths Longitudinal studies surfaces and bony bony defects for increase clinical attachment level may increase recession. defects, reduces probing debridement Lack of i a After 5 years, greatest reduction in probin ack of professional depths, facilitates plaque Apically repositioned flap years, 9 maintenance and depth with osseous Tecontouring. ‘ ; with or without bony . . . restorative and cosmetic recontouring Apically repositioned flap with or without dentistry . bony recontouring used in crown- Gingivectomy lengthening procedures to provide biologic patient compliance can be detrimental to long- term success. ee 3Certain systemic tetracyclines, notably doxycycline, are safe an d 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 elevated collagenase activity, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL rather than function as an antimicrobial. 207 Personal and Provider Approaches to Oral Health these delivery systems are relative- ly new, there is a paucity of evi- dence addressing their long-term effectiveness. For patients who have lost sig- nificant bone and/or connective tis- sue, there are a number of regener- ation procedures to facilitate the growth of new periodontal liga- ment, 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; allo- grafts, which use bone grafts from a human donor, and xenografts, which use tissues from other species. Limited case report evi- dence shows that extraoral auto- genous 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 improve- ments 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 periodon- tics. Freeze-dried demineralized bone is an allograft material, har- vested, prepared, and demineral- ized prior to grafting. The deminer- alization step is important because it retains the activity of bone mor- TABLE 8.1l2a Odds ratios for risk factors for oral and pharyngeal cancers Both Sexes Males — Females Cigarettes: Never 1.0 1.0 Ever 19 3.0 Smoking status, adjusted for alcohol drinking? None 1.0 1.0 Short duration/former 14 4.0 1 to 19 per day for 20+ years 1.6 3.0 20 to 39 per day for 20+ years 2.8 4.4 40+ per day for 20+ years 44 10.2 Cigars? Never 1.0 _ Ever 2.8 _ Pipes? Never 1.0 _ Ever 18 _— Smokeless tobacco among nonsmokers! Never _ 1.0 Ever _— 6.2 Number of drinks of beer per week, adjusting for smoking? <1 10 1.0 1to4 1.2 2.2 5to 14 17 29 15 to 29 3.4 23 30+ 47 18.0 Number of drinks of hard liquor per week, adjusting for smoking?