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PubMed1991

Autoimmunity in periodontal disease.

Periodontal disease in characterized by the loss of the normal supporting tissues of the teeth and a humoral and cellular immune response to bacterial antigen of dental plaque which accumulates at the dento-gingival junction. This review considers the evidence for the existence of an autoimmune component of the host immune response, the possible origin of such a response and the way in which such a host response may contribute to the changes observed in the periodontium in the disease.

Autoantigens↗

PubMed1976

[Correlations between chronic liver diseases and periodontal diseases with special reference to animal experiments].

The purpose of the present paper was to investigate possible relationships between chronic liver diseases and marginal periodontal diseases, using clinical and radiographic methods as well as animal experiments. The periodontal conditions of 100 patients with histologically confirmed chronic hepatopathies were compared with those in a control group of same size. The results of these studies testify unequivocally to unfavourable conditions in the group of hepatopaths. This finding is corroborated and complemented by subsequent animal experiments. The difference in the extent and intensity of the periodontal alterations between a group of Wistar rats with experimentally induced hepatopathies and a control group was statistically significant. These results permit the conclusion that an aetiologic relation between chronic hepatopathies and marginal periodontal diseases may be assumed.

Animals↗

PubMed1992

Multi-level statistical models in studies of periodontal diseases.

Periodontal data typically have a hierarchical structure, with sites grouped within individuals, and individuals grouped within communities. Also, the occasion may be regarded as another level since the acquired knowledge indicates that periodontal disease activity may vary over time. Conventional statistical tests are based on unilevel analysis of data. However, this approach to statistical analysis is often inconvenient in periodontal research because of the variation in the outcome variables between the various levels in the hierarchy. Lately there have been important developments in the statistical theory which have made available powerful statistical techniques for analyzing multilevel or hierarchical data. This report describes a new approach for analyzing periodontal data and uses an illustrative example to build a model which explains part of the variability in the response variable. The results from this analysis are then compared to results from an earlier report which uses unilevel methods and the findings discussed. The present multilevel approach has several advantages over unilevel methods, mainly due to its statistical validity and efficiency. Further, it permits the incorporation of explanatory variables measured at the site and the subject levels, and those which vary across the time points. Multilevel analyses have a promising potential and are expected to have a significant impact on periodontal research.

Age Factors↗

PubMed1993

Monoclonal antibodies to lipopolysaccharide of four oral bacteria associated with periodontal disease.

Periodontal disease is a common inflammatory disease which erodes the supporting structures of the teeth, and is initiated by a subgingival infection with selected Gram-negative bacteria. Monoclonal antibodies (mAb) to lipopolysaccharide (LPS) of four periodontal pathogens, A. actinomycetemcomitans, P. intermedia, F. nucleatum and P. gingivalis were examined for specificity and their ability to bind these pathogens in a particle concentration fluorescence immunoassay (PCFIA). The mAb selected were specific for their homologous bacteria and when tested against a large battery of other bacteria, including 16 genera and 46 species, were found not to cross-react with heterologous species. When each of the mAb was challenged with 40 or more homologous freshly isolated bacteria, more than 90% were positive. Non-cellular antigens in the form of soluble LPS and extracellular vesicles were examined for their ability to bind to assay components and alter the apparent results of the assay. LPS was found to have potential as an interfering agent if bound to assay components prior to sample treatment, but this non-specific binding was significantly reduced when a surfactant was added to the buffers. Extracellular vesicles had no significant effect on the estimation of P. gingivalis by the assay.

Aggregatibacter actinomycetemcomitans↗

PubMed1991

[Biological markers in periodontal disease].

Periodontal diseases are thought to occur in an episodic manner with periods of breakdown and remission. This phenomenon can differ from one site to another. Clinical indices are unable to provide useful information about disease activity, but certain biologic markers may reflect periods of breakdown of connective tissue component of the periodontium. Procaryotic markers were excluded because they are difficult to identify and the results were uncertain. Tissue breakdown factors within the gingival sulcus were examined. Some of these factors could be correlated with the active stages of disease. These include: mediators of inflammation, catabolic enzymes, and enzymes associated with tissue necrosis. Among the eucaryotic tissue components, one or several could be of use to the dentist to assay disease activity. These tests could conceivably be done without complex and expensive equipment and could offer a new diagnosis index, "the active site index."

Biomarkers↗

PubMed1990

[Polynuclear neutrophils and periodontal diseases].

Periodontal diseases are bacteria associated diseases. The host response to these bacteria is critical. Non specific defense mechanisms are mainly mediated by the polymorphonuclear neutrophil which out numbers the others crevicular leucocytes. This paper reviews the beneficial and possible detrimental aspect of the neutrophil functions.

Bacterial Adhesion↗

PubMed1997

The role of Actinobacillus actinomycetemcomitans in the pathogenesis of periodontal disease.

Periodontal disease consists of a constellation of complex bacterium-host cell interactions. One example of these oral pathogens, Actinobacillus actinomycetemcomitans, has an arsenal of putative virulence determinants that account for its potent periodontopathogenicity. Of these determinants, invasion of host cells and leukocytotoxicity have been studied extensively.

Actinobacillus Infections↗

PubMed1997

Respiratory burst of neutrophils in diabetic patients with periodontal disease.

Periodontal disease, a frequent complication of diabetes mellitus, is the major cause of tooth loss. However, studies on neutrophil function in patients with this condition have yielded contradictory findings. The NADPH oxidase activity of 40 diabetic patients with periodontosis who were on metabolic control was evaluated and compared with that in 40 healthy subjects. Superoxide anion production was measured by a photometric method, with NBT reduction at 490 nm in a microplate reader and by a microscopic method, with a percentage of positive PMNs with granules of formazan in the cytoplasm. When the PMN respiratory burst was activated by phorbol myristate acetate (PMA), a protein kinase C (PKC) soluble activator, superoxide production of diabetics (4.31 +/- 1.67 A x 10(-3)/min) and normal subjects (4.25 +/- 1.25 A x 10(-3)/min) was comparable by photometric method, whereas a significantly defective response to opsonized zymosan was observed when the microscopic method was used (58 +/- 17% in diabetics and 66 +/- 18% in controls; p = 0.05). Therefore in patients with diabetes the impact on PMN function is of multifactorial origin, and is probably correlated to the glucose level and to glycation of PMN protein, such as NADPH oxidase or myeloperoxidase. Alternatively, glucose in PMN may be reduced by aldose reductase to polyols, and this pathway requires NADPH, the coenzyme for the respiratory burst. Moreover, we found that superoxide production in response to opsonized zymosan was reduced in diabetic patients. The activation of protein tyrosine kinase (PTK) is an important mechanism underlying transmembrane signaling and, moreover, protein tyrosine phosphorylations, stimulated by zymosan receptor-mediated activation, might be caused by the activation of specific PTK, whereas activation by PMA is probably mediated through another PKC type.

Chemotaxis, Leukocyte↗

PubMed2001

Periodontal disease and periodontal management in patients with cancer.

Periodontal infection may exacerbate during cancer therapy and may result in oral pain and infection, and systemic infection, which may cause morbidity and can lead to mortality in neutropenic cancer patients. Periodontal disease in head and neck cancer patients treated with radiation therapy may lead to acute and chronic complications. The literature was reviewed by a search of Medline of the National Library of Medicine. The search was conducted to identify publications assessing periodontal disease in cancer patients. In addition, a review of papers referenced in the retrieved papers was conducted to identify additional publications for review. Periodontal disease should be assessed and managed prior to medical treatment of cancer for those with oropharyngeal cancer, and for patients in whom neutropenia may develop during treatment. Pretreatment assessment and management, and maintenance of oral hygiene have been shown to be effective in preventing oral and systemic complications during treatment. A complete oral and periodontal examination is appropriate for all patients planned to receive head and neck radiation therapy and those to be treated with medical protocols that are anticipated to result in neutropenia. Oral and periodontal care must continue following cancer therapy, and requires that the health care provider have an understanding of the malignant disease, oral manifestations of the disease, medical management of the disease, and of the oral complications that may develop.

Antibiotic Prophylaxis↗

PubMed2001

[Risk factors that modulate periodontal diseases].

Periodontal diseases now is a chronic inflammatory disease caused by Gram negative bacterial infection. Recently, it is of interest to evaluate risk factors that modulate initiation and development of this disease. A recent study have suggested that obesity is one of the risk factors. In this regard, most recently, we found that leptin, a regulator of food intake and whole-body energy metabolism, acts as a negative regulator of LPS-induced expression of inflammatory cytokines of macrophages via inhibition of NF-kB.

English Abstract↗

PubMed2004

Destructive membranous periodontal disease (ligneous periodontitis): a case report and 3 years follow-up.

Destructive membranous periodontal disease is a rare, destructive and poorly defined entity, which is the part of a systemic disease due to plasminogen deficiency and fibrin deposition. The disease is characterised by gingival enlargement and periodontal tissue destruction that leads to rapid tooth loss despite treatment attempts. Biopsy is essential to rule out other periodontal disease in the differential diagnosis.

Adult↗

PubMed1998

Molecular epidemiology of oral treponemes associated with periodontal disease.

Periodontitis, a disease responsible for tooth loss worldwide, is characterized by chronic inflammation of the periodontium, eventually leading to destruction of periodontal ligaments and supporting alveolar bone. Spirochetes, identified by dark-field microscopy as being the most predominant bacteria in advanced lesions, are thought to play a causative role. Various spirochetal morphotypes were observed, but most of these morphotypes are as yet uncultivable. To assess the role of these organisms we designed oligonucleotide probes for the identification of both cultivable and so far uncultivable spirochetes in periodontitis patients. Subgingival plaque specimens taken from diseased sites (n = 200) and healthy control sites (n = 44) from 53 patients with rapidly progressive periodontitis (RPP) were submitted to direct in situ hybridization or dot blot hybridization after prior amplification with eubacterial primers. Spirochetes were found in all patients, but their distributions varied considerably. Parallel use of oligonucleotide probes specific for cultivable or so far uncultivable treponemes suggested the presence of novel yet unknown organisms at a high frequency. These uncultivable treponemes were visualized by fluorescence in situ hybridization, and their morphologies, sizes, and numbers could be estimated. All RPP patients included in this study harbored oral treponemes that represent either novel species, e.g., Treponema maltophilum, or uncultivable phylotypes. Therefore, it is necessary to include these organisms in etiologic considerations and to strengthen efforts to cultivate these as yet uncultivable treponemes.

Adult↗

PubMed1992

[Diabetic disease and periodontal disease. Diabetes and periodontopathy].

Diabetic patients have been reported to be more susceptible to gingivitis and periodontitis than healthy subjects, and these diseases are commonly considered to be oral complications of diabetes. The influence of diabetes on the onset and development of periodontal disease has been studied for many years but clear agreement is still lacking on the nature of the relationship between diabetes and these oral disorders. In fact recent observational epidemiological studies suggest that diabetes should not be considered as the direct cause of periodontal disease but rather as a systemic promoting factor, able to produce conditions suitable for local agents producing gingivitis and periodontitis. The overriding oral problem in diabetes is infection, like with any of the dermal lesions in the diabetic. In fact periodontal disease is caused by specific bacteria (Bacteroides Gingivalis, Actinobacillus actinomycetemcomitans) growing in the periodontal pocket so that the bacterial products such as histolytic enzymes, endotoxins or exotoxins may exert a direct effect. Particular attention has been directed to the neutrophils and to their role in antibacterial defense. In fact a reduced phagocytosis, leukotaxis and leucocyte index have been reported in neutrophils from diabetics. The careful metabolic control was reported by most of the Authors to lower the incidence and to reduce the severity of periodontal disease. This may be related both to the improvement in leukocyte function and to a change in gingival fluid rendering it less suitable for bacterial growth. In diabetics also local factors, such as decreased pH of salivary fluid and a reduced salivary flow, seem to play an important role.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1997

The effects of smoking on periodontal disease and periodontal therapies.

Cigarette smoking is a significant risk factor for the development of periodontal disease. In addition, there is an association between a reduced healing response subsequent to various periodontal therapies and cigarette smoking. As providers of dental care, it is our responsibility to inform our patients of the deleterious effects of smoking as well as the benefits of the cessation of this habit.

Adult↗

PubMed1997

CD29 expression on CD4+ gingival lymphocytes supports migration of activated memory T lymphocytes to diseased periodontal tissue.

The cell surface phenotypes of CD+ cells extracted from inflammatory periodontal disease tissues were analyzed using two- and three-color immunofluorescence and flow cytometry. Cells extracted from both adult periodontal and localized juvenile periodontitis lesions showed a depressed CD4/CD8 ratio (1.0 +/- 0.1 adult periodontitis and 1.1 +/- 0.1 localized juvenile periodontitis) compared with cells recovered from normal/marginal gingivitis tissue (1.8 +/- 0.2) or with normal peripheral blood cells (2.1 +/- 0.1) or periodontal disease blood cells (2.1 +/- 0.1 and 1.7 +/- 0.1 for adult periodontitis and juvenile periodontitis, respectively). The monoclonal antibodies anti-2H4 and anti-4B4 were used to identify the CD45RA and CD29 antigens respectively on CD4+ T cells from the periodontal disease lesions. In peripheral blood. CD29+ cells accounted for 66-77% of the CD4+ population, and CD45RA+ cells accounted for 22-27% of the CD4+ subset. No differences in expression were found between peripheral blood lymphocytes from normal subjects and from periodontal disease patients. Two-color analyses of lymphocytes from periodontal diseased tissues showed that 87-89% of the CD4+ population were CD29+ and that 70-79% of the CD4+ cells were CD45RA+. Normal tissues contained significantly fewer CD4+CD29+ cells (56 +/- 4%) and CD4+CD45RA+ cells (40 +/- 4%) on average, and few, if any double-labelled cells could be accounted for. These data implied that a significant percentage of the CD4+ cells from the diseased tissues were both CD29+ and CD45RA+ and that these populations are found in quite different proportions in diseased periodontal tissue than in peripheral blood or nondiseased tissue. In further analyses using three-color cytometry the mean percentage of CD4+ CD29+ CD45RA+ lymphocytes extracted from periodontal disease lesions was 43 +/- 9% of the CD4+ population. These results suggest that CD4+ T lymphocytes in periodontal disease not only demonstrate varying levels of maturity but also that the accumulation of CD4+ T cells within the periodontal tissues may be a result of increased adhesion and transendothelial migration.

Adult↗

PubMed2001

Current concepts and future trends for periodontal disease and periodontal therapy, Part 2: Classification, diagnosis, and nonsurgical and surgical therapy.

As noted in both this and the previous review, our understanding of the etiology, diagnosis, and treatment of the periodontal diseases is continuously evolving. Periodontology in the year 2001 is different than what it was 20 years ago, and the specialty will be different 20 years in the future. Assessment of patients will be more specific, and the development of risk profiles will allow identification of individuals who require greater or lesser amounts of care. Therapy can then be directed to the specific needs of each patient. Surgical periodontics will be focused on regeneration, not resection. Lastly, as patients continue care on a maintenance schedule, their status will be assessed by sensitive tests that will predict the onset of an active phase of disease so that appropriate interceptive treatment can be provided.

Anti-Bacterial Agents↗

PubMed2001

Potential associations between chronic respiratory disease and periodontal disease: analysis of National Health and Nutrition Examination Survey III.

BACKGROUND: Associations between poor oral health and chronic lung disease have recently been reported. The present study evaluated these potential associations by analyzing data from the National Health and Nutrition Examination Survey III (NHANES III), which documents the general health and nutritional status of randomly selected United States subjects from 1988 to 1994. METHODS: This cross-sectional, retrospective study of the NHANES III database included a study population of 13,792 subjects > or = 20 years of age with at least 6 natural teeth. A history of bronchitis and/or emphysema was recorded from the medical questionnaire, and a dichotomized variable combined those with either chronic bronchitis and/or emphysema, together considered as chronic obstructive pulmonary disease (COPD). Subject lung function was estimated by calculating the ratio of forced expiratory volume (FEV) after 1 second (FEV1)/forced vital capacity (FVC). Oral health status was assessed from the DMFS/T index (summary of cumulative caries experience), gingival bleeding, gingival recession, gingival probing depth, and periodontal attachment level. Unweighted analyses were used for initial examination of the data, and a weighted analysis was performed in a final logistic regression model adjusting for age, gender, race and ethnicity, education, income, frequency of dental visits, diabetes mellitus, smoking, and alcohol use. RESULTS: The mean age of all subjects was 44.4 +/- 17.8 years (mean +/- SD): COPD = 51.2 +/- 17.9 years and subjects without COPD = 43.9 +/- 17.7 years. Subjects with a history of COPD had more periodontal attachment loss than subjects without COPD (1.48 +/- 1.35 mm versus 1.17 +/- 1.09 mm, P = 0.0001). Subjects with mean attachment loss (MAL) > or = 3.0 mm had a higher risk of COPD than those having MAL < 3.0 mm (odds ratio, 1.45; 95% CI, 1.02 to 2.05). A trend was noted in that lung function appeared to diminish with increasing periodontal attachment loss. CONCLUSIONS: The findings of the present analysis support recently published reports that suggest an association between periodontal disease and COPD.

Adult↗

PubMed2001

Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses?

Inflammatory bowel disease (IBD) comprises two chronic, tissue-destructive, clinical entities Crohn disease (CD) and ulcerative colitis (UC) both apparently caused by immunological overreaction (hypersensitivity) to commensal gut bacteria. Under normal conditions the intestinal immune system shows a down-regulating tone ('oral tolerance') against dietary antigens and the indigenous microbiota. This local homeostasis is disturbed in IBD, leading to hyperactivation of T helper 1 (Th1) cells with abundant secretion of interferon-gamma and tumor necrosis factor (TNF) and production of IgG antibodies against commensal bacteria. In addition, UC includes genetically determined autoimmunity, particularly IgG1-mediated cytotoxic epithelial attack. Breaching of the epithelium is the best-defined event underlying abrogation of oral tolerance, but immune deviation caused by cytokines fiom irritated epithelial cells or subepithelial elements (for example, mast cells, natural killer cells, macrophages) may also be involved. Endogenous infection with local hypersensitivity likewise causes periodontal disease, reflecting 'frustrated' immune elimination mechanisms entertained by antigens from dental plaque. Altogether, perturbation of a tightly controlled cytokine network, with abnormal crosstalk between several cell types, apparently explains the progressive immunopathology of chronic inflammatory mucosal diseases in general. This adverse development will be influenced by numerous immunity genes, the dosage and potential pathogeniciy of commensal bacteria, general health, nutritional status, and psychological factors. Several targets for new therapy have tentatively been identified to block immunopathological mechanisms in IBD, and inhibition of TNF has a striking beneficial effect in CD, supporting a central role of this cytokine.

Animals↗