Global oral health inequalities: task group--periodontal disease.

Periodontal diseases constitute one of the major global oral health burdens, and periodontitis remains a major cause of tooth loss in adults worldwide. The World Health Organization recently reported that severe periodontitis exists in 5-20% of adult populations, and most children and adolescents exhibit signs of gingivitis. Likely reasons to account for these prevalent diseases include genetic, epigenetic, and environmental risk factors, as well as individual and socio-economic determinants. Currently, there are fundamental gaps in knowledge of such fundamental issues as the mechanisms of initiation and progression of periodontal diseases, which are undefined; inability to identify high-risk forms of gingivitis that progress to periodontitis; lack of evidence on how to prevent the diseases effectively; inability to detect disease activity and predict treatment efficacy; and limited information on the effects of integration of periodontal health as a part of the health care program designed to promote general health and prevent chronic diseases. In the present report, 12 basic, translational, and applied research areas have been proposed to address the issue of global periodontal health inequality. We believe that the oral health burden caused by periodontal diseases could be relieved significantly in the near future through an effective global collaboration.

An economic evaluation of a chlorhexidine chip for treating chronic periodontitis: the CHIP (chlorhexidine in periodontitis) study.

BACKGROUND: The authors previously suggested that an adjunctive, controlled-release chlorhexidine, or CHX, chip may reduce periodontal surgical needs at little additional cost. This article presents an economic analysis of the CHX chip in general dental practice. METHODS: In a one-year prospective clinical trial, 484 chronic periodontitis patients in 52 general practices across the United States were treated with either scaling and root planing, or SRP, plus any therapy prescribed by treating, unblinded dentists; or SRP plus other therapy as above but including the CHX chip. Economic data were collected from bills, case report forms and 12-month treatment recommendations from blinded periodontist evaluators. RESULTS: Total dental charges were higher for SRP + CHX chip patients vs. SRP patients when CHX chip costs were included (P = .027) but lower when CHX chip costs were excluded (P = .012). About one-half of the CHX chip acquisition cost was offset by savings in other charges. SRP + CHX chip patients were about 50 percent less likely to undergo surgical procedures than were SRP patients (P = .021). At the end of the trial, periodontist evaluators recommended similar additional procedures for both groups: SRP, about 46 percent; maintenance, about 37 percent; surgery, 56 percent for SRP alone and 63 percent for SRP + CHX chip. CONCLUSIONS: Adjunctive CHX chip use for general-practice patients with periodontitis increased costs but reduced surgeries over one year. At study's end, periodontists recommended similar additional surgical treatment for both groups. CLINICAL IMPLICATIONS: In general practice, routine use of the CHX chip suggests that costs will be partially offset by reduced surgery over at least one year.

Treatment of periodontitis by local administration of minocycline microspheres: a controlled trial.

BACKGROUND: Periodontitis is an inflammatory condition of tooth-supporting tissues that is usually treated by mechanical removal of plaque and microorganisms that adhere to teeth. This treatment, known as scaling and root planing, is not optimally effective. Adjunctive therapy with locally delivered antimicrobials has resulted in improved clinical outcomes such as probing depth reduction. This article reports on the efficacy and safety of locally administered microencapsulated minocycline. METHODS: Seven hundred forty-eight (748) patients with moderate to advanced periodontitis were enrolled in a multi-center trial and randomized to 1 of 3 treatment arms: 1) scaling and root planing (SRP) alone; 2) SRP plus vehicle; or 3) SRP plus minocycline microspheres. The primary outcome measure was probing depth reduction at 9 months. Clinical assessments were performed at baseline and 1, 3, 6, and 9 months. RESULTS: Minocycline microspheres plus scaling and root planing provided substantially more probing depth reduction than either SRP alone or SRP plus vehicle. The difference reached statistical significance after the first month and was maintained throughout the trial. The improved outcome was observed to be independent of patients' smoking status, age, gender, or baseline disease level. There was no difference in the incidence of adverse effects among treatment groups. CONCLUSIONS: Scaling and root planing plus minocycline microspheres is more effective than scaling and root planing alone in reducing probing depths in periodontitis patients.

Low prevalence of a periodontitis-associated interleukin-1 composite genotype in individuals of Chinese heritage.

BACKGROUND: Polymorphisms in the interleukin-1 (IL-1) gene cluster have been associated with an increased risk of developing certain diseases. A specific composite genotype of IL-1A and IL-1B polymorphisms, consisting of allele 2 of both IL-1A +4845 and IL-1B +3954 (formerly +3953) has been associated with an increased risk of severe adult periodontitis. Approximately 30% of the European population carry this genotype. The prevalence of the above IL-1A and IL-1B composite genotype in populations of different ethnic origins is unknown. Therefore, the primary aim of this study was to determine the prevalence of the IL-1 composite genotype in individuals of Chinese heritage, since epidemiologic studies indicate that periodontitis is widespread among ethnic Chinese. An additional aim was to evaluate if there was an association between the composite genotype and the severity of periodontal disease. METHODS: A convenience sample of 300 volunteers of Chinese heritage (ages 21 to 69 years) received a periodontal examination including full-mouth clinical attachment loss measurements, probing depths, plaque index scores, and bleeding on probing. Blood was collected from a fingerstick and placed on a blotting paper card. The blood samples were analyzed for IL-1A +4845 and IL-1B +3954 polymorphisms using polymerase chain reaction (PCR)-based methods. RESULTS: Only 7 of the 300 subjects (2.3%) carried the composite IL- 1 genotype consisting of allele 2 of both IL-1A +4845 and IL-1B +3954. Allele 2 of the IL-1A +4845 polymorphism was carried by 17.0% (51/300) of the subjects; of these, only 2 were homozygous. Allele 2 of the IL-1B +3954 polymorphism was much rarer with only 3.3% (10/300) of the study population carrying this marker. All of the people who carried the IL-1B polymorphism were heterozygous. Too few of the subjects were positive for the IL-1 composite genotype to establish any relationship with the susceptibility to periodontitis. CONCLUSIONS: It was concluded that the prevalences of both IL-1A and IL-1B polymorphisms are dramatically lower in Chinese than those reported for Europeans. Findings from this study bring into question the usefulness of the composite genotype of allele 2 of both IL-1A +4845 and IL-1B +3954 as a method for determining the susceptibility of Chinese patients to adult periodontitis.

Periodontal infections and cardiovascular disease--how strong is the association?

In the past decade there has been renewed interest in the old hypothesis that infections increase the risk of developing cardiovascular disease and stroke. There is now a convincing body of evidence that atherosclerosis has a major inflammatory component and is much more than the simple vascular accumulation of lipids. Infectious agents that have been linked to an increased risk of coronary heart disease (CHD) include Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses. The concept has emerged that each of these agents is an independent risk factor for CHD and that common chronic infections are important. In addition, periodontal infections have also been implicated as one of several factors contributing to the development of CHD. Evidence supporting a causative role of chronic infections in CHD is largely circumstantial. However, the evidence is sufficiently strong to warrant further examination of the possible link between chronic infections and CHD. In this review the lines of evidence for a causative role of C. pneumoniae in the development of CHD are summarized and contrasted with the lines of evidence suggesting a periodontal infection--CHD association. If common or widespread chronic infections are truly important risk factors for CHD, it is unlikely that a single infection will be shown to be causative. It is likely that the entire microbial burden of the patient from several simultaneous chronic infections is more important (e.g., H. pylori-caused gastric ulcers + C. pneumoniae-caused bronchitis + periodontitis). Increased cooperation between cardiologists and periodontists will be required to determine if, and what, combinations of common chronic infections are important in the pathogenesis of CHD and stroke.

Development of a classification system for periodontal diseases and conditions.

Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings, including: (1) considerable overlap in disease categories, (2) absence of a gingival disease component, (3) inappropriate emphasis on age of onset of disease and rates of progression, and (4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Figure 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.

Development of a classification system for periodontal diseases and conditions.

Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings including: 1) considerable overlap in disease categories, 2) absence of a gingival disease component, 3) inappropriate emphasis on age of onset of disease and rates of progression, and 4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Fig. 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.

A mucosal irritancy test device for intraoral use in dogs.

The objective of this investigation was to conduct, in dogs, a 6-hour acute mucosal irritation study of a new bioerodible treatment. The main problem was to retain the test drug in situ without extraneous irritation from the retention device. A buccal cup was machined from acrylic with a chamber capacity of 0.025 ml and a flange that could be ligated to a tooth. Ten female retired breeder beagles, 7 to 8 years old, with naturally occurring moderate periodontitis were examined and the upper canine teeth scaled to remove plaque and calculus. One week later the buccal cups were placed at the gingival margin of the upper canine teeth and fixed in place with wire ligature passing through holes in the flange and around the tooth, engaging shallow nicks made in the enamel near the gingival margin so the wire would not slide up and down. The buccal cup was further stabilized with glass ionomer cement placed on the crown and over the outer surface of the cup. Buccal cups were loaded with test, placebo, or no ointment by technicians in a scheme to which examiners were blind. Hourly examinations were made, and after 6 hours the cups were removed and gingival mucosa scored for irritation by a previously described method. All dogs tolerated the test and retained the cups for 6 hours. There was no mucosal irritation from the empty cups. We conclude that this new device can be used successfully for testing new agents for short-term mucosal irritancy.

Biochemical alterations in inflammatory periodontal diseases I. Poly (ADP-ribose) synthetase activity in gingiva and gingival fibroblasts from humans with periodontitis.

Periodontal diseases are characterized in part by generation of oxygen free radicals, which can cause breaks in cellular DNA strands. Repair of damaged DNA is dependent upon the synthesis of poly (ADP-ribose)(PADPR) catalyzed by PADPR synthetase, an enzyme known to be activated by the broken ends of DNA strands. We measured the activities of PADPR synthetase and of PADPR glycohydrolase, which degrades PADPRS, in gingival biopsy specimens from 16 sites with adult periodontitis and 12 clinically healthy control sites. The results indicated that sites with periodontitis displayed markedly reduced PADPR synthetase activity compared with healthy control sites, whereas PADPR glycohydrolase activity was not changed. The mean specific activity of PADPR synthetase for the diseased specimens was one-sixth of that of the healthy specimens (p < 0.001). The PADPR synthetase activity was negatively correlated with the Gingival Index (rs = -0.60), pocket depth (rs = -0.70) and bleeding upon probing (rs = -0.72). Cultured fibroblasts derived from clinically characterized healthy and diseased gingival sites reflected similar patterns of enzyme activity. The mean specific activity of PADPR synthetase for the diseased-site cultures (n = 9) was 56 +/- 7% (p < 0.001) of the cultures from healthy control sites (n = 6). These results suggest that a reduced level of PADPR synthetase activity is associated with increased inflammation and periodontal destruction, and that the ability to synthesize PADPR is compromised in adult periodontitis.

Comparison of a sonic and a manual toothbrush for efficacy in supragingival plaque removal and reduction of gingivitis.

A new sonic electric toothbrush (Sonicare) and a traditional manual toothbrush were compared for efficacy in removing supragingival plaque and reducing gingival inflammation in a 12-week, single-blind clinical trial. 60 subjects with a gingival index (GI) of > 1.5 and no probing depths > 5 mm were randomly assigned to use either the manual or sonic brush, instructed in its use, and asked to brush each morning and evening for 2 minutes. Plaque scores were taken at baseline and at 1, 2, 4, and 12 weeks using the Turesky modification of the Quigley-Hein plaque index. Gingival inflammation was assessed by the GI, bleeding tendency score, presence or absence of bleeding on probing, volumetric measurements of gingival crevicular fluid (GCF), and aspartate aminotransferase (AST) levels in GCF. Repeated measures multivariate analyses of variance were used to detect time- and device-dependent differences for all clinical assessments between the 2 groups over the 5 visits. Both types of brush were effective in removing supragingival plaque. The sonic brush was statistically superior, on a percentage reduction basis, in removing supragingival plaque from the dentition taken as a whole (F-statistic; p = 0.012) and was particularly better in hard-to-reach areas such as posterior teeth (F-statistic; p = 0.003) and interproximal sites (F-statistic; p = 0.004). Both devices were equally effective in reducing gingival inflammation. The sonic brush exhibited less tendency to cause gingival abrasion than the manual brush (1 incident with sonic, 5 incidents with manual), confirming the safety of this product as an oral hygiene device.

Development of a drug delivery system for the treatment of periodontal disease based on bioerodible poly(ortho esters).

Poly(ortho esters) prepared by the condensation of 1,2,6-hexanetriol and an alkyl orthoacetate are viscous, semisolid materials at room temperature that can be injected using a blunt needle. When tetracycline was incorporated into these materials, complete release occurred within about 24 hours, but when small amounts of Mg(OH)2 were incorporated into the polymer release could be extended to many weeks, and a loading of 0.5 wt% resulted in sustained release of about 10 days. When adhesion was tested using bovine teeth, cohesive failure of the pure polymer occurred at a force of about 392 mN cm-2 and cohesive failure of a polymer incorporating 10 wt% tetracycline and 1 wt% (Mg(OH)2 occurred at about 118 mN cm-2. The combination of injectability, dentoadhesiveness and ability to control accurately the release of incorporated antibiotics makes these materials promising candidates for bioerodible delivery systems useful in the treatment of periodontitis. Toxicological studies are currently in progress.

Longitudinal evaluation of elastase as a marker for the progression of periodontitis.

To determine whether elastase levels in gingival crevicular fluid (GCF) could serve as a marker for the progression of periodontitis, we monitored GCF elastase and periodontal status in selected sites in 32 periodontally healthy volunteers and 31 periodontitis patients at intervals over a 6-month period. Clinical measurements included plaque index, gingival index, bleeding on probing, suppuration, probing depth, clinical attachment level, and relative attachment level measured with an automated disk probe. GCF elastase, detected by reaction with a fluorescent substrate, was assessed visually against fluorescence standards and quantitatively with a fluorometer. Bone loss was detected by subtraction radiography of standardized vertical bite-wing radiographs at baseline and 6 months. Mean visual elastase scores (VES) and quantitative elastase measurements were significantly higher (P < 0.001) in sites from periodontitis patients than in sites from healthy volunteers. When bone loss was used as the criterion for disease progression, significantly higher (P < 0.001) visual and quantitative GCF elastase levels were found at progressing sites than in nonprogressing sites in the periodontitis patients. The odds ratios (OR) for the event of developing bone loss with positive 4-minute and 8-minute VES tests were 4.2 (P < 0.001) and 7.4 (P < 0.001), respectively. When corrected for the tendency of progressing sites to be clustered within a subpopulation of patients, the OR for developing bone loss with the 4-minute and 8-minute VES tests were 3.1 (P < 0.007) and 4.9 (P < 0.001), respectively. These data indicate that sites with high levels of elastase are at significantly greater risk for progressive bone loss as assessed by digital subtraction radiography.

Langerhans cells in oral mucosa of rhesus monkeys before and after infection by simian retrovirus-1 and simian immunodeficiency virus.

To study the influence of experimental infection with simian retrovirus-1 and simian immunodeficiency virus on the number and distribution of Langerhans cells in oral mucosa of rhesus monkeys, 10 monkeys were intravenously inoculated with simian retrovirus-1, 7 with simian immunodeficiency virus, and 2 were mock-inoculated. Biopsies were taken from gingiva and cheek pouch before infection and at 1 (simian immunodeficiency virus group only), 4, and 7 months after infection. Langerhans cells were detected in frozen sections by immunohistochemistry with monoclonal antibodies Leu-6 and HLA-DR. The mean number of Langerhans cells per surface millimeter and square millimeter of epithelium was calculated under blind conditions. The results showed no statistically significant differences in the number or distribution of Langerhans cells in the three groups at the various time points of examination. Similarly, no differences were detected within any group over the observation period. Thus systemic infection of rhesus monkeys with either simian retrovirus-1 or simian immunodeficiency virus does not lead to a significant change in the number of Langerhans cells in oral mucosal epithelium.

Diagnostic tests for periodontal diseases.

A high level of interest in the development of diagnostic tests capable of detecting factors associated with progressing ("active") periodontal disease has continued in the past year. Notable advances and refinements have occurred in subtraction radiographic techniques and in the development of computer-linked, controlled-force periodontal probes. Development and evaluation of new diagnostic tests have also proceeded at a rapid pace. Particular emphasis has been placed on rapid tests for putative periodontal pathogens and detection in gingival crevicular fluid of host-derived enzymes. An intense effort must be made to determine the clinical value of diagnostic tests in longitudinal studies that use state-of-the-art assessments of disease progression.

Effects of ascorbic acid depletion and supplementation on periodontal health and subgingival microflora in humans.

This study describes the relationship between varying ascorbate intake, periodontal status, and subgingival microflora as part of a multidisciplinary investigation of ascorbic acid (AA) metabolism in young men housed for 13 weeks in a nutrition suite that provided controlled periods of ascorbic acid depletion and repletion. Twelve medically healthy non-smoking men, aged 25 to 43 years, ate a rotating four-day diet adequate in all nutrients except ascorbic acid. Following an initial baseline period during which the subjects received 250 mg AA/day, the subjects received 5 mg AA/day for a 32-day depletion period. Eight of the 12 subjects participated in a subsequent 56-day repletion period designed to replace the reduced body AA pool slowly. Plasma and leukocyte ascorbate levels, Plaque Index, Gingival Index, probing depths, and attachment level were monitored at the beginning and end of the depletion and repletion periods. Subgingival plaque samples were obtained and examined for selected organisms by indirect immunofluorescence microscopy. A uniform oral hygiene program was reinforced after each examination. Ascorbate concentrations in plasma and leukocytes responded rapidly to changes in vitamin C intake. There were no significant changes in plaque accumulation, probing pocket depth, or attachment level during the study. In contrast, gingival bleeding increased significantly after the period of AA depletion and returned to baseline values after the period of AA repletion. However, no relationship could be demonstrated between either the presence or proportion of target periodontal micro-organisms and measures of bleeding or ascorbate levels.