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Dental plaque revisited: bacteria associated with periodontal disease.

Between 3-12 weeks after the beginning of supragingival plaque formation, a distinctive subgingival microflora predominantly made up of gram-negative, anaerobic bacteria and including some motile species, becomes established. In order to establish in a periodontal site, a species must be able to attach to one of several surfaces including the tooth (or host derived substances adhering to the tooth), the sulcular or pocket epithelium, or other bacterial species that are attached to these surfaces (Socransky and Haffajee 1991). Bacterial adhesion has demonstrated specificity in the mechanisms involved and studies have shown that there is a diversity of receptors on tooth surfaces, epithelial or other host cells and other bacteria. Recent studies have described bacterial complexes that are present in subgingival plaque and these studies are likely to help in current understanding of the complex ecology observed in dental plaque biofilm (Socransky, Haffajee et al. 1998). Bacterial interactions play important roles in species survival. Some interspecies relationships are favourable, in that one species produces growth factors for, or facilitates attachment of, another species. Other relationships are antagonistic due to competition for nutrients and binding sites, or to the production of substances that limit or prevent the growth of another species (Socransky and Haffajee 1991). A number of different bacterial interactions within plaque biofilm have been discussed. In the last 30-40 years, a vast amount of evidence has been published to suggest that bacteria are the primary aetiological agents of periodontal diseases. In the 1950s and early 1960s, periodontal treatment was based on the non-specific plaque hypothesis. However, the non-specific plaque hypothesis gave way after studies suggested that not all organisms in plaque are equally capable of causing destructive periodontal disease. Thus the concept of specificity re-emerged. Criteria for defining periodontal pathogens have been developed and include association, elimination, host response, virulence factors, animal studies and risk assessment (Haffajee and Socransky 1994). Until recently there were few consensus periodontal pathogens and trying to discriminate pathogenic from non-pathogenic species has been a difficult task for dental researchers for a variety of reasons. A discussion of the specific microbiota associated with gingivitis, chronic and aggressive periodontitis, NUG, HIV-associated periodontitis and implantitis has been presented. The bacteria associated with periodontal diseases are predominantly gram-negative anaerobic bacteria and may include A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus, C. rectus, E. nodatum, P. micros, S. intermedius and Treponema sp. The bacterial numbers associated with disease are up to 10(5) times larger than those associated with health.

Animals↗

The antimicrobial treatment of periodontal disease: changing the treatment paradigm.

Over the last 100 years, methods of surgical periodontal treatment have enjoyed a history of success in improving oral health. The paradigm of care is based on the "non-specific plaque hypothesis"--that is, the overgrowth of bacterial plaques cause periodontal disease, and the suppression of this overgrowth reduces disease risk. The central feature of this approach to care is the removal of inflamed gingival tissue around the teeth to reduce periodontal pocket depth, thereby facilitating plaque removal by the dentist and by the patient at home. Over the last 30 years, with the recognition that periodontal disease(s) is caused by specific bacteria and that specific antimicrobial agents can reduce or eliminate the infection, a second paradigm has developed. This new paradigm, the "specific plaque hypothesis", focuses on reducing the specific bacteria that cause periodontal attachment loss. The contrast between the two paradigms can be succinctly stated as follows: The antimicrobial therapy reduces the cause, while the surgical therapy reduces the result of the periodontal infection. The specific plaque hypothesis has two important implications. First, with the increasing attention to evidence-based models for prevention, treatment, outcome assessment, and reimbursement of care, increasing attention and financial effort will be channeled into effective preventive and treatment methods. Second, the recent observations that periodontal infections increase the risk of specific systemic health problems, such as cardiovascular disease, argue for the prevention and elimination of these periodontal infections. This review highlights some of the evidence for the specific plaque hypothesis, and the questions that should be addressed if antimicrobial agents are to be used responsively and effectively.

Anti-Bacterial Agents↗

Inhibition of bone DNA and collagen production by surface-associated material from bacteria implicated in the pathology of periodontal disease.

Gentle extraction of oral bacteria implicated in the pathogenesis of periodontal disease, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, or Eikenella corrodens, with saline removes the extracellular components while leaving the bacteria intact. This readily-solubilized surface-associated material (SAM) has been demonstrated to significantly inhibit DNA and collagen synthesis by murine calvaria at concentrations as low as 10 ng/ml. DNA and collagen synthesis in isolated calvarial osteoblasts were also inhibited by these SAM preparations with similar dose responses. The inhibitory effect of these bacterial expolymers was blocked by 1 microM indomethacin. The potent inhibitory actions on bone synthesis of the SAM from these bacteria may contribute to the alveolar bone loss found in patients with periodontal disease.

Aggregatibacter actinomycetemcomitans↗

Diagnosis of periodontal diseases.

This article provides an overview of currently available periodontal diagnostic methods. It also addresses several prototype test kits undergoing in-office evaluations. Diagnostic techniques are critically evaluated in light of current concepts regarding the etiology and pathogenesis of periodontal disease. Furthermore, suggestions are made with regard to strategies for using multiple diagnostic assays.

Alveolar Bone Loss↗

Mandibular dysfunction and periodontitis. A comparative study of patients with periodontal disease and occlusal parafunctions.

Fifty-one patients (mean age, 47.3 years) with moderate to severe periodontal disease and 40 patients (mean age, 48.9 years) with symptoms related to bruxism (occlusal parafunctions such as grinding and/or clenching of the teeth) were compared with regard to periodontal conditions and signs and symptoms of mandibular dysfunction. The bruxists reported more symptoms of pain and dysfunction of the masticatory system than the periodontal patients. The clinical dysfunction index was significantly higher among the bruxists, while there was a similarity between the groups in the variation of occlusal conditions, except for occlusal wear, which was more pronounced in the bruxist group. Attrition was in general positively correlated to alveolar bone height. This correlation was stronger (and statistically significant) for the canines than for other teeth. Attrition was negatively correlated to tooth mobility. It is concluded that patients with moderate to severe periodontal disease and patients with bruxism/occlusal parafunctions are distinctly different with regard to signs and symptoms of mandibular dysfunction. The results support the opinions that there is no or only weak correlation between periodontal disease and bruxism, and between bruxism and occlusal status.

Adult↗

Periodontal disease in ancient populations.

Recent clinical and anthropological findings indicate that the conventional concept of the pathogenesis of periodontal disease requires review. The periodontal lesion has been defined as a generalised horizontal loss of crestal bone resulting from host immune and inflammatory responses triggered by the action of commensal bacteria, and the extension of gingivitis into the deeper periodontium to become periodontitis has been assumed to occur slowly but steadily over many years. Anthropological and clinical investigations reveal that the widespread loss of crestal tissue is relatively unusual and that lesions of the alveolus are commonly localised and severe. Longitudinal studies have shown that the disease progresses in bursts and is stable in both the gingivitis and periodontal modes in between the burst activity. The findings of the present study demonstrate that generalized horizontal periodontitis has been unusual and has not been responsible for tooth loss. Other factors responsible for deficient alveolar margins in dry bones have been overlooked in most studies, leading to overassessment of the incidence of periodontal disease in postmortem materials; the same assumptions have led to overassessment of periodontal disease in clinical studies and practice.

Anthropology, Physical↗

An update on HIV and periodontal disease.

With the advent of newer pharmacological approaches to the treatment of human immunodeficiency virus (HIV) infection, the incidence and progression of both atypical and conventional periodontal diseases are changing. The incidence of necrotizing periodontitis and gingival diseases of fungal origin appears to be on the decline as a result of these therapies that have led to increased life spans for HIV patients. However, in cases where these therapies lose their effectiveness and HIV patients relapse into an immunosuppressed state, these conditions may recur. Recent evidence has shown that HIV patients with more conventional periodontal diseases such as chronic periodontitis may have increased attachment loss and gingival recession when compared to their HIV-negative counterparts. This pattern of loss of periodontal support may be due in part to a diffuse invasion of opportunistic bacterial infections, viruses, and fungi into the gingival tissue, leading to a more elevated and more diffuse destructive inflammatory response in the periodontal soft and hard tissues. While the accepted approaches to treating the spectrum of periodontal diseases in HIV patients remain essentially unchanged over the past 15 years, the impact of newer systemic therapies on patient immunocompetence may influence treatment decisions.

Candidiasis, Oral↗

Gingival crevicular fluid gelatinase and its relationship to periodontal disease in human subjects.

Collagenolytic enzymes released by neutrophils are associated with the destruction of periodontium in periodontal diseases. Measurement of these enzymes in gingival crevicular fluid (GCF) could be used to test for periodontal diseases and thereby simplify diagnosis. To test this hypothesis, gelatinase (MMP-9) was analyzed in GCF samples with a simple assay system. GCF was collected by a mouthrinse method from 10 patients with gingivitis (G); 10 well-treated and maintained periodontitis patients (TP) without detectable loss of attachment; and 9 patients with recurrent loss of periodontal attachment (greater than 2 mm) and/or abscess formation (RP). Clinical measurements including tooth mobility (MOB) and gingival attachment level (GAL) were made monthly for a maximum of 10 months. Active and latent forms of gelatinase were measured by a functional assay using gelatin substrate-gel enzymography and the activities were quantified by laser densitometry. Reproducibility analysis demonstrated that the assay (inter-gel, inter-assay, inter-scan) and diurnal variations were small compared to biological variation. The presence of active gelatinase was detected in 97.8% of TP samples, 86.4% of RP samples, but in only 11.4% of G samples. In addition, the mean active gelatinase activity was found to be significantly higher (p less than 0.001) in the RP (71,006 U) than the TP (43,814 U) groups, both of which were higher (p less than 0.001) than the G group (2824 U). During periods of attachment loss, samples from the RP group exhibited a 2-fold increase of mean active gelatinase activity (129,414 U).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Periodontal disease and general health.

There is considerable interest in the possible relationship between periodontal disease and pregnancy complications, cardiovascular disease, diabetes and respiratory diseases. This interest has been stimulated by data obtained from epidemiological studies and a better understanding of the pathogenesis of periodontal disease. Whilst much of the data support an association between oral and general health, further studies are needed to accept or reject a causal relationship.

Cardiovascular Diseases↗

Experimental gingivitis in relation to susceptibility to periodontal disease. (I.) Clinical observations.

The aim of the present study was to investigate the rate of development of experimentally-induced gingival inflammation in relation to the susceptibility to periodontal disease. By selection according to age, a younger (25-39 years) and an older (45-54 years) age group, with a comparable reduced but healthy periodontium, was selected. This equal amount of periodontal breakdown may suggest that the younger age group represented individuals with a relatively higher degree of susceptibility to periodontal disease. At the start of the experiment, each patient was instructed to abstain from oral hygiene procedures in 1 quadrant of the mouth for a period of 18 days. Results showed that all subjects developed signs of gingival inflammation. Regarding the development of redness and swelling, no differences could be assessed between the 2 age groups. However, analysis of the bleeding scores revealed that bleeding on probing developed more rapidly in the younger age group. It was concluded that those patients who have suffered from a more rapid form of periodontal disease also develop inflammation, in terms of bleeding on probing, more rapidly.

Adult↗

The effect of supragingival plaque control on the progression of advanced periodontal disease.

The aim of the present trial was to study the effect of meticulous supragingival plaque control on (i) the subgingival microbiota, and (ii) the rate of progression of attachment loss in subjects with advanced periodontal disease. An intra-individual group of sites exposed to non-surgical periodontal therapy served as controls. 12 patients with advanced periodontal disease were subjected to a baseline examination (BL) including assessments of oral hygiene status, gingival condition (BoP), probing depth, clinical attachment level and subgingival microbiota from pooled samples from each quadrant. The assessments were repeated after 12, 24 and 36 months. Following BL, a split mouth study was initiated. The patients received oral hygiene instruction, supragingival scaling and case presentation. 2 quadrants in each patient were identified as "test" and the remaining 2 as "control" quadrants. Subgingival therapy was performed in all bleeding sites in the control quadrants. Oral hygiene instructions and plaque control exercises were repeated once every 2 weeks during the initial 3 months of the study. Thereafter the plaque control program was repeated once every 3 months for the duration of the 3 years. Sites demonstrating loss of clinical attachment > or =2 mm in the test quadrants were treated subgingivally. The results showed that in both test and control quadrants repeated oral hygiene instructions and supragingival plaque removal procedures resulted in low plaque scores throughout the study. The gingival bleeding scores and the frequency of periodontal pockets > or =4 mm was, however, significantly higher in the test quadrants than in the control quadrants. At the end of the 3 year study, the control quadrants showed significantly more reduced (> or =2 mm) pockets than the test quadrants, 265 versus 96. The number of sites in the test quadrants showing probing attachment loss > or =2 mm was more than 4x greater than in the control quadrants (59 versus 13). The microbiological findings indicate a more pronounced reduction only for P. gingivalis in the control quadrants. None of the other 4 marker bacteria consistently reflected or predicted the clinical parameters. The present study shows that only supragingival plaque control fails to prevent further periodontal tissue destruction in subjects with advanced periodontal disease.

Adult↗

Management of periodontal disease in older patients.

As the "graying of America" is accelerating, so is the incidence and severity of periodontal diseases. The clinical management of periodontal disease in an aging population is becoming an increasingly important issue for dental professionals. This article reviews age-associated risk actors that can contribute to loss of periodontal attachment. The influence of age-related systemic conditions and medications upon clinical management is also discussed.

Age Factors↗

Frequency distribution of individuals aged 20-70 years according to severity of periodontal disease experience in 1973 and 1983.

The aim of this study was to compare changes in periodontal status of a Swedish population over a 10-year period expressed as frequency distributions of individuals according to severity of periodontal disease experience. The study involved 600 randomly selected individuals evenly distributed into age groups 20, 30, 40, 50, 60 and 70 years, examined in 1973 and another randomly selected group of 597 individuals similarly age distributed and examined in 1983. Based on clinical data and full mouth intraoral radiographs all individuals were classified into 5 groups according to severity of periodontal disease experience. In 1983, 23% of the individuals were classified as having healthy periodontal tissues, group 1, compared to 8% in 1973. The changes were most pronounced in the age groups 20 and 30 years, among whom 58% and 35%, respectively, were registered as having healthy periodontium in 1983. The prevalence of individuals with gingivitis without signs of lowered periodontal bone level, group 2, was 22% in 1983 compared to 41% in 1973. In all, 49% of the dentate population in 1973 and 45% in 1983 showed no marginal alveolar bone loss. Moderate periodontal bone loss, group 3, was found in 41% of the population in 1983 compared to 47% in 1973. Among 30-, 40-, and 50-year-olds, there were more, and among 60- and 70-year-olds, fewer individuals in this group in 1983 compared to 1973. 96% of the dentate population were classified as belonging to groups 1, 2 or 3 in 1973 compared to 86% in 1983.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

An epidemiologic study of the relationship between various states of occlusion and the pathological conditions of dental caries and periodontal disease.

This study explored relationships between dental caries and periodontal disease and either (1) any of 8 existing orthodontic indices or (2) any of 41 individual cephalometric measures. The 486 subjects examined revealed no clinically significant associations between any of the disease measures and either the indices or the cephalometric measurements.

Adolescent↗

Tobacco smoking and neutrophil activity in patients with periodontal disease.

BACKGROUND: Tobacco smoking has considerable negative effects on periodontal health. The mechanisms behind these effects are incompletely understood but may be related to the host response. The aim of the present study was to investigate the influence of tobacco smoking on the gingival crevicular fluid (GCF) levels of elastase, lactoferrin (LF), alpha-1-antitrypsin (alpha-1-AT), and alpha-2-macroglobulin (alpha-2-MG) under periodontally diseased conditions. METHODS: The study population included 15 smokers (5 women and 10 men) aged 34 to 69 years and 17 non-smokers (5 women and 12 men) aged 31 to 81 years. Clinical registration of gingival index (GI), plaque index (PI), probing depth, as well as sampling of GCF were made at 3 sites with severe lesions and 3 sites with moderate lesions in each individual. The elastase activity was measured with a chromogenic low molecular substrate and the LF, alpha-1-AT, and alpha-2-MG concentrations with ELISA. RESULTS: The results showed that, with regard to severe lesions, smokers had a significantly lower concentration of alpha-2-MG as well as significantly lower total amounts of alpha-2-MG and alpha-1-AT than non-smokers. With regard to moderate lesions, smokers tended to exhibit a lower concentration of alpha-2-MG, but the difference was not statistically significant. Comparing moderate and severe lesions, smokers exhibited no gradual increase with disease severity in contrast to non-smokers, who showed significantly or almost significantly increased levels of LF and alpha-2-MG in severe as compared to moderate lesions. CONCLUSIONS: The present results indicate that the levels of alpha-2-MG and alpha-1-AT are suppressed in smokers with periodontitis, suggesting that smoking interferes with these protease inhibitors. This may be one mechanism by which smoking affects the inflammatory response.

Adult↗

Lesions of the oral mucosa and periodontal disease behavior in pregnant patients.

AIMS: A study is made to contrast the prevalence and severity of periodontal disease, the needs for periodontal treatment, and the prevalence of lesions of the oral mucosa in pregnant (study group) and non-pregnant women. STUDY DESIGN: During the period 1991-1999, a prospective observational study was made of 7952 women seen in the Dental School of De La Salle Bajío University (Leon, Gto. Mexico). The following variables were documented: age, disease antecedents, simplified periodontal index, and lesions of the oral mucosa. Two patient groups were defined: pregnant and non-pregnant women exhibiting a similar age distribution. The data were presented as percentages, and comparisons were made based on the chi-square test. RESULTS: Pregnancy was not found to be a decisive factor for the development of periodontal disease, no differences in the prevalence of gingivitis (54.54 and 50.50%) and periodontitis (31.82 and 31.75%) being observed between the two groups. However, the severity of periodontitis was significantly greater among the pregnant women (18.18% versus 9.88%; p< 0.01). The prevalence of oral mucosal lesions was similar in both groups (30%), 13 lesions being identified in the study group, with a predominance of leukoedema, traumatic ulceration, red traumatic lesions, benign migratory glossitis (geographic tongue), irritative keratosis and pyogenic granuloma. The non-pregnant women in turn exhibited 57 lesions. Pyogenic granuloma and benign migratory glossitis exhibited significant differences between the two groups (p< 0.005). CONCLUSIONS: Gingivitis and periodontitis showed similar prevalences in pregnant and non-pregnant women, though severe periodontitis was more frequent among the former. Pyogenic granuloma and benign migratory glossitis were the lesions with the greatest prevalences during pregnancy.

Adolescent↗

Susceptibility and risk factors in periodontal disease.

Epidemiological studies demonstrate a high prevalence of advanced destruction but also that relatively few individuals in each age group account for most of the advanced periodontal disease. The available data suggest that three quarters of advanced periodontal disease could be prevented by targeting an effective preventive strategy on the 28% of individuals especially at risk. Questions remain regarding: 1) whether an acceptable cost-effective preventive strategy can be devised; and 2) whether it is possible to establish a simple method of identifying the 'at risk' group. The various risk factors are numerous and include systemic diseases, smoking, drug therapy, hormonal disturbances and genetic factors as well as the more mundane factors such as plaque control and socio-economic and education and attitude factors. Aside from these factors, many patients present with periodontal disease and have no discernible predisposition other than possibly genetic, for which we can not currently test, and for the vast majority of patients there would appear to be no other alternative to periodic thorough examination for all patients, early treatment of all periodontal lesions and appropriate dental health education.

Adult↗