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Risk of severe periodontal disease in a Swedish adult population. A cross-sectional study.

In this study, potential risk factors for severe periodontal disease were identified in a cross-sectional sample from the county of Jonkoping, Sweden. 547 adults 20-70 years of age were categorised clinically and radiographically by level of periodontal disease experience. These levels were used to divide the sample into groups--individuals without any reduction in periodontal bone level (60%) and those with severe periodontal bone loss (13%)--which were then used in univariate and multivariate logistic regression analyses as dependent variable. Demographic, socio-economic, general health, smoking habits, clinical, and dental care variables were used in the different regression analyses. In the univariate model, age (20-70 years) was found to be correlated with more severe periodontal disease experience (odds ratio: 1.13; 95% CI: 1.10-1.17). The association with periodontal disease was more pronounced for the older age groups (50, 60, and 70 years). A negative financial situation was also related to severe periodontal bone loss when regressed univariately (odds ratio 2.20 [95%: 1.04-4.68]). Moderate-heavy smoking (> or =10 cigarettes/day) appeared to be associated with severe periodontal destruction with an odds ratio of 9.78 (95% CI: 3.62-36.42). Of the clinical variables in the univariate model, higher mean levels of supragingival dental plaque and the presence of subgingival calculus were related to more severe periodontal disease with odds ratios of 1.02 (95%: 1.01-1.03) and 2.96 (95%: 1.50-5.88), respectively. When the same variables were regressed multivariately, age (continuous) (odds ratio 1.17 [95% CI: 1.12-1.22]), moderate-heavy smoking (odds ratio 11.84 [95% CI: 4.19-33.50]), and higher mean levels of plaque (odds ratio 1.02 [95% CI: 1.00-1.03]) remained significant. Light smoking (1-9 cigarettes/day) was not significantly associated with severe periodontal disease in the 2 regression models. The present study demonstrated that smoking, greater age, and higher mean levels of plaque are potential risk factors for severe periodontal disease in this specific population.

Adult↗

The potential role of bacteria and their antigens in periodontal disease.

The inflammatory changes typical of periodontal disease are believed to involve immunological reactions, with bacteria being a potential source of the antigens inducing these reactions, with bacteria being a potential source of the antigens inducing these reactions. Various investigators have studied the ability of specific organisms to induce tissue changes in experimental animals, while others have examined human sera and tissues for the presence of antibodies reacting with particular organisms or their isolated antigens. The significance of these results is assessed, particularly with respect to the problem of antibody cross-reactivity. The antigens that could be involved in periodontal disease are discussed in terms of the difference in structure of Gram-positive and Gram-negative bacterial cells, with attention being drawn to those components that could occur extracellularly and thus diffuse into oral tissues. The antigen most studied is the lipopolysaccharide or endotoxin of Gram-negative cells which, through the mediation of complement, is a potential inflammatory agent.

Adhesiveness↗

Update on plaque and periodontal disease.

The relationship between plaque and inflammatory periodontal disease is complex, and requires extensive and often abstruse research. One unfortunate consequence is that much relevant information concerning this relationship is not readily available to those most concerned with the prevention and treatment of inflammatory periodontal disease. The present review is concerned with some relevant developments in recent plaque research.

Dental Calculus↗

Herpesviruses in human periodontal disease.

Recent studies have identified various herpesviruses in human periodontal disease. Epstein-Barr virus type 1 (EBV-1) infects periodontal B-lymphocytes and human cytomegalovirus (HCMV) infects periodontal monocytes/ macrophages and T-lymphocytes. EBV-1, HCMV and other herpesviruses are present more frequently in periodontitis lesions and acute necrotizing ulcerative gingivitis-lesions than in gingivitis or periodontally healthy sites. Reactivation of HCMV in periodontitis lesions tends to be associated with progressing periodontal disease. Herpesvirus-associated periodontitis lesions harbor elevated levels of periodontopathic bacteria, including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteriodes forsythus, Prevotella intermedia, Prevotella nigrescens and Treponema denticola. It may be that active periodontal herpesvirus infection impairs periodontal defenses, thereby permitting subgingival overgrowth of periodontopathic bacteria. Alteration between latent and active herpesvirus infection in the periodontium might lead to transient local immunosuppression and explain in part the episodic progressive nature of human periodontitis. Tissue tropism of herpesvirus infections might help explain the localized pattern of tissue destruction in periodontitis. Absence of herpesvirus infection or viral reactivation might explain why some individuals carry periodontopathic bacteria while still maintaining periodontal health. Further studies are warranted to delineate whether the proposed herpesvirus-periodontopathic bacteria model might account for some of the pathogenic features of human periodontal disease.

Bacteria, Anaerobic↗

[The etiopathogenesis of periodontal diseases: the role of microorganisms. A review].

The microbiology of periodontal diseases as well as associations between certain microorganisms and types/stages of periodontal diseases are discussed and the ecology and the composition of the subgingival plaque are included in this discussion, too. Furthermore, the possible role of microorganisms associated with periodontal diseases, their pathogenic mechanisms and their virulence factors are treated in the present article. Periodic upsets of the host-parasite equilibrium seem to be responsible for the bursts of disease progression. Several plaque hypotheses (specific, non-specific, opportunistic) have been proposed as likely models to explain the nature of periodontal infections and diseases. However, none of these theories is widely accepted at the moment. Therefore, we suggest that further investigations concerning the complex bacterial interactions and the manner in which the host responds to the mass and the composition of the dental plaque must be carried out in the future.

Adolescent↗

Environmental tobacco smoke and periodontal disease in the United States.

OBJECTIVES: Cigarette smoking is a leading risk factor for periodontal disease. This cross-sectional study investigated the relation between environmental tobacco smoke (ETS) and periodontal disease in the United States. METHODS: Data were obtained from the Third National Health and Nutrition Examination Survey (1988-1994). The outcome was periodontal disease, defined as 1 or more periodontal sites with attachment loss of 3 mm or greater and a pocket depth of 4 mm or greater at the same site. Exposure to ETS at home and work was self-reported. The study analyzed 6611 persons 18 years and older who had never smoked cigarettes or used other forms of tobacco. RESULTS: Exposure to ETS at home only, work only, and both was reported by 18.0%, 10.7%, and 3.8% of the study population, respectively. The adjusted odds of having periodontal disease were 1.6 (95% confidence interval = 1.1, 2.2) times greater for persons exposed to ETS than for persons not exposed. CONCLUSIONS: Among persons in the United States who had never used tobacco, those exposed to ETS were more likely to have periodontal disease than were those not exposed to ETS.

Adolescent↗

Alternative methods for screening periodontal disease in adults.

Clinical measurements of periodontal attachment loss, while not always representing the histological changes, are used to establish the diagnosis of adult periodontitis. Such measurements are difficult to perform accurately and are labor intensive. To counter these problems, index teeth and index sites have been employed in an attempt to estimate the severity of the periodontal condition without the need to resort to elaborate attachment measurements. Unfortunately, such indices usually tend to underestimate prevalence while often overestimating severity. The purpose of the present study was to examine the correlation of alternative clinical, radiographic and microbiological parameters, with periodontal disease using the diagnostic criteria of established periodontitis. 508 adults included in this study received thorough periodontal examination which included probing pocket depth, clinical attachment level, plaque, gingival and calculus scores, together with radiographic analysis and assays of subgingival periopathogenic microorganisms. Radiographic alveolar bone loss and probing pocket depth had the highest correlation with clinical attachment loss (phi = 0.72 and phi = 0.75 respectively). Plaque scores (phi = 0.17), like gingival scores (phi = 0.06) and calculus scores (phi = 0.42) had poor correlation with established periodontitis. Periodontopathogenic species demonstrated high specificity and negative predictive values; but low sensitivity and positive predictive values make for an overall low correlation of these species with established periodontitis. However, when used in a logistic regression model, the presence of P. gingivalis (odds ratio = 6.25) has shown to contribute significantly to the estimate of probability for established periodontitis. The use of these various alternative parameters for screening of periodontal disease is discussed in light of their sensitivity, specificity and predictive value.

Adult↗

Early carotid atherosclerosis in subjects with periodontal diseases.

BACKGROUND AND PURPOSE: There is growing experimental evidence implicating chronic inflammation/infection as an atherosclerotic risk factor. In this study, the involvement of periodontal disease in the development of early atherosclerotic vascular lesions has been evaluated. METHODS: In randomly chosen 82 patients with periodontal disease and 31 periodontally healthy individuals subjected to a clinical oral examination in 1985, atherosclerotic risk factor analysis and carotid ultrasonography was performed during reexamination 16 years later. Common carotid artery intima-media thickness (IMT) and lumen diameter were measured and intima-media area (cIMA) was calculated. The relationship between IMT and cIMA as dependent variables and periodontal disease, age, gender, body mass index, heredity for atherosclerosis, diabetes mellitus, hypertension, plasma cholesterol, smoking, and education as independent variables was evaluated in a multiple logistic regression model. RESULTS: The mean values of IMT and cIMA were significantly higher in patients with periodontal disease than in controls, both at the right (P<0.01 and P<0.001, respectively) and left side (P<0.001 for both variables). When the means of the bilateral measurements of these 2 ultrasonographic variables were tested, multiple logistic regression analysis identified periodontal disease as a principal independent predictor of the common carotid artery cIMA (odds ratio [OR], 5.20; P=0.003) and IMT (OR, 4.64; P=0.004). CONCLUSIONS: The present results indicate that periodontal disease is associated with the development of early atherosclerotic carotid lesions.

Adult↗

The relationship between microbiological assays and the clinical signs of periodontal disease.

Ninety-five patients with periodontal disease each had subgingival plaque samples collected from four sites (one from each quadrant) in their mouths. The relative proportions of spirochaetes, motile rods and cocci were determined using dark field microscopy and the proportion of anaerobic to aerobic micro-organisms calculated after culture. In addition, clinical recordings were made. The only significant correlations observed were between probing depth or attachment loss and the proportion of cocci in the plaque (negative association), probing depth or attachment loss and sites which were suppurating or displayed a radiolucent interdental crest (positive association), and the percentage of cocci and sites with a radiolucent interdental crest (negative association). Partial correlation analysis controlling for probing depth or attachment loss showed that a significant inverse association between the percentages of cocci and the presence of a radiolucent interdental crest remained. No significant associations were observed between clinical signs such as bleeding on probing or suppuration and the microbiological assays. Overall there was a poor correlation between many of the signs thought by some to indicate periodontal disease activity.

Adult↗

The role of histopathology in the diagnosis and prognosis of periodontal diseases.

The histological evaluation of surgical biopsies from affected tissues is a standard way of assessing pathological change and determining treatment in many diseases. In most forms of periodontal disease, however, this approach finds limited application. Here, we review what uses the histopathological approach has in the study and evaluation of the periodontal diseases. Current understanding of the changes in epithelial anatomy during pocket formation, the cellular composition and dynamics of the inflammatory infiltrate and the mechanisms of bone resorption and repair are reviewed from the perspective of the information available from microscopical investigation, including the uses and potential application of modern immunocytochemical methods to these questions. The usefulness of histological study of biopsy material is reassessed in the light of advances made in immunohistochemical techniques and their application to gingival inflammatory infiltrates and epithelia. Such techniques offer immediately valuable research opportunities with potential for diagnostic applications, noteably the recognition of phases of destructive activity and their differentiation from periods of effective host defence.

Gingiva↗

Epidemiology of periodontal disease: a review and clinical perspectives.

The purpose of this paper is to assimilate epidemiological evidence for the prevalence of periodontal disease in human populations, and for comprehensive understanding of the disease for health care providers. Periodontal disease is a pathological condition affecting the supporting structures of teeth. It is characterised by a bacterial challenge that can instigate a destructive host response leading to periodontal attachment loss, bone loss and ultimately, possible tooth loss. The specifics of the disease process are obscured by our incomplete understanding of the role of various risk factors. Periodontal epidemiology literature lacks consistency in methodology of research, which includes various definitions for periodontal disease and health; different approaches to measuring periodontal indices of pocket depth, and attachment loss; inconsistent study designs and lack of adjustments to known risk factors. These inconsistencies do not allow for effective comparison of epidemiological studies, which is essential to find strong associations of risk factors with periodontal disease, which in turn is necessary for the interpretation of risk and causality. This paper will address several areas within the topic of periodontal disease epidemiology, including definitions of periodontal disease instituted by researchers, approaches to epidemiological studies in periodontitis, and risk factors in periodontal disease. Consideration is given to aspects of design and analyses relevant to evaluation of reports in the literature. For the clinical practitioner this review provides a theoretical framework to approach patients with comprehensive knowledge of not only the disease presentation, but also the environmental factors that govern past history, present condition and future response to treatments and interventions.

Alveolar Bone Loss↗

Diagnostic biomarkers for oral and periodontal diseases.

This article provides an overview of periodontal disease diagnosis that uses clinical parameters and biomarkers of the disease process.This article discusses the use of biomarkers of disease that can be identified at the tissue, cellular, and molecular levels and that are measurable in oral fluids such as saliva and gingival crevicular fluid. Biomarkers identified from these biologic fluids include microbial, host response, and connective tissue-related molecules that can target specific pathways of local alveolar bone resorption. Future prospects for oral fluid-based diagnostics that use micro-array and microfluidic technologies are presented.

Bacteria↗

Is there an association between periodontal disease, prematurity and low birth weight? A population-based study.

BACKGROUND: The relationship between periodontal diseases in pregnancy and children born prematurely or with low birth weight has been increasingly investigated, showing inconclusive results. OBJECTIVES: To test the link between periodontal disease in pregnant women and low birth weight or prematurity. METHODS: A population-based, cross-sectional study was carried out in Southern Brazil. The sample consisted of 449 parturients who were interviewed and examined up to 48 h post-partum. Three outcomes were investigated: low birth weight, prematurity and prematurity and/or birth weight. Periodontal disease, the exposure, was defined as (i) at least one site with a periodontal pocket; (ii) the presence of pockets at four or more sites. Socio-demographic information relating to health and maternal habits was collected through a questionnaire and by hospital medical records. Simple and multiple regression analysis was performed. FINDINGS: There was no statistically significant association between periodontal disease and low birth weight. Periodontal pocket was not associated with low birth weight and/or pre-term birth after being adjusted. A periodontal pocket in at least one site was associated with prematurity (odds ratio=2.6; 95% confidence interval 1.0-6.9) even after adjusting for maternal schooling, parity, number of previous children of low birth weight, number of pre-natal consultations and body mass index. After the introduction of variables relating to maternal health during pregnancy, this association disappeared. CONCLUSIONS: No association was found between periodontal disease in the mother and the low birth weight. An association between prematurity and periodontal pockets was found but it was confounded by maternal health variables.

Adolescent↗

Periodontal disease and upper genital tract inflammation in early spontaneous preterm birth.

OBJECTIVE: To estimate the relationship between maternal periodontal disease and both early spontaneous preterm birth and selected markers of upper genital tract inflammation. METHODS: In this case-control study, periodontal assessment was performed in 59 women who experienced an early spontaneous preterm birth at less than 32 weeks of gestation, in a control population of 36 women who experienced an early indicated preterm birth at less than 32 weeks of gestation, and in 44 women with an uncomplicated birth at term (>or = 37 weeks). Periodontal disease was defined by the degree of attachment loss. Cultures of the placenta and umbilical cord blood, cord interleukin-6 levels, and histopathologic examination of the placenta were performed for all women. RESULTS: Severe periodontal disease was more common in the spontaneous preterm birth group (49%) than in the indicated preterm (25%, P =.02) and term control groups (30%, P =.045). Multivariable analyses, controlling for possible confounders, supported the association between severe periodontal disease and spontaneous preterm birth (odds ratio 3.4, 95% confidence interval 1.5-7.7). Neither histologic chorioamnionitis, a positive placental culture, nor an elevated cord plasma interleukin-6 level was significantly associated with periodontal disease (80% power to detect a 50% difference in rate of histological chorioamnionitis, alpha = 0.05). CONCLUSION: Women with early spontaneous preterm birth were more likely to have severe periodontal disease than women with indicated preterm birth or term birth. Periodontal disease was not associated with selected markers of upper genital tract inflammation. LEVEL OF EVIDENCE: II-2

Adult↗

Salivary aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase: possible markers in periodontal diseases?

BACKGROUND: Saliva can be used as a diagnostic fluid in medicine. Components of saliva proposed as disease markers include enzymes (alkaline phosphatase, esterase, glucuronidase, aminopeptidase), immunoglobulins (IgA, IgG), and hormones (steroid hormones). Many of these salivary components appeared to be useful biochemical markers of the evolution of periodontal disease, for which salivary analysis can offer a cost-effective approach for monitoring the disease. The salivary components proposed as markers for periodontal disease activity are aspartate aminotransferase (AST), alkaline phosphatase (ALP), aminopeptidases, and glucuronidases. The purpose of our study was to illustrate the influence of periodontal disease on the level of salivary AST, alanine aminotransferase (ALT) and ALP. METHODS: All clinical periodontal examinations were performed by the same periodontist. All patients included in the study presented a probing depth >5 mm, bleeding on probing and alveolar bone loss >40%. Salivary AST, ALT and ALP activities were measured using DiaSys analysis kits from Diagnostic Systems. The methods were adapted for saliva. RESULTS: Salivary AST activity in patients with periodontal disease was significantly increased (p<0.01) (median 81.75+/-23 U/L) compared with controls (15.25+/-10.5 U/L). Salivary ALT activity was not significantly modified in saliva from patients with periodontal disease compared with the control group. Our results showed a significant (p<0.01) increase in salivary ALP activity (34.38+/-1.5 U/L) in patients with periodontal disease compared with controls (6.6+/-4.2 U/L). CONCLUSIONS: Our results revealed that periodontal destruction such as periodontal pockets, gingival bleeding and suppuration are related to higher ALP and AST levels in saliva. Salivary AST could be used as a useful marker for monitoring periodontal disease. The increase in salivary ALP activity in periodontitis demonstrated could be associated with alveolar bone loss, a key feature of periodontal disease. More studies are necessary to evaluate which specific clinical, microbiological and histological characteristics of periodontal disease are associated with elevated levels of AST and ALP in saliva.

Adult↗

Tobacco smoking and periodontal diseases.

There is a growing body of scientific evidence indicating that nicotine contributes to the progression of periodontal disease, and is detrimental to healing following periodontal therapy. Smokers show a higher prevalence and greater severity of periodontal disease than non-smokers. Nicotine has toxic effects on peripheral, circulation, which cause gingival vasoconstriction. As a result, a decreased number of immune cells are available in the gingival tissue, which translates into a weakened defence-reparative system. Nicotine can also depress primary and secondary immune response by reducing the chemotactic and phagocytic activities of leukocytes. Clinically, smoking has been associated with increased pocket depths, calculus deposition,alveolar bone loss, acute necrotizing ulcerative gingivitis, and osteoporosis in postmenopausal women. Despite efforts by various investigators, the precise mechanisms underlying the effects of smoking on periodontal status and wound healing remain unresolved. This paper reviews the relationship between smoking and periodontal disease. It also includes a historical overview of the research, and a review of the effects of smoking on oral bacteria, the immune system and exocrine glands. In addition, risk assessment for periodontal disease, clinical features of smokers' periodontitis, response of smokers' periodontal disease to treatment, and ideas for future research are discussed.

Age Factors↗

[Calcium and the risk for periodontal disease].

Recently, there is much interest regarding the relationship between periodontal disease and the life style as well as systemic disease including osteoporosis. In addition, there is increasing awareness that dietary calcium intake and other nutrients are important for prevention and management of periodontal disease. In this paper, a cross-sectional study from NHANES III for investigating the association between dietary calcium intake and periodontal disease is introduced, and the management of periodontal disease is proposed from nutritional aspects.

English Abstract↗