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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Periodontitis has been linked to clinical cardiovascular disease but not to subclinical atherosclerosis. The purpose of this study was to determine whether periodontitis is associated with carotid artery intima-media wall thickness (IMT). Cross-sectional data on 6017 persons aged 52 to 75 years were obtained from the Atherosclerosis Risk in Communities Study 1996 to 1998 examination. The dependent variable was carotid IMT >/=1 mm. Periodontitis was defined by extent of attachment loss >/=3 mm: none/mild (<10%), moderate (10% to <30%), or severe (>/=30%). Covariates included age, sex, diabetes, LDL cholesterol, HDL cholesterol, triglycerides, hypertension, smoking, waist-hip ratio, education, and race/study center. Odds of IMT >/=1 mm were higher for severe periodontitis (OR 2.09, 95% CI 1.73 to 2.53) and moderate periodontitis (OR 1.40, CI 1.17 to 1.67) compared with no periodontitis. In a multivariable logistic regression model, severe periodontitis (OR 1.31, CI 1.03 to 1.66) was associated with IMT >/=1 mm, while adjusting for the other factors in the model. These results provide the first indication that periodontitis may play a role in the pathogenesis of atheroma formation, as well as in cardiovascular events.
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PMID:Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study. 1170 71

Diabetes mellitus is an important disease of the endocrine system. Many studies have associated this disease to the pathogenesis and the severity of periodontal disease. The aim of this article is to illustrate the relation between diabetes mellitus and periodontal disease. Many studies show an important association between diabetes and the pathogenesis of periodontal disease. Vascular changes caused by hyperglycemia are associated to the development of periodontal pathogens species. Moreover diabetics show an exacerbate host response with hyperproduction of inflammatory mediators and polymorphonuclear dysfunction. Diabetics with good metabolic control and patients with good oral hygiene show a reduced risk of periodontitis. In conclusion, diabetes mellitus (IDDM and NIDDM) is an important risk factor for periodontitis. Odds Ratio is 3. Diabetes mellitus determines changes in bacterial population and production of inflammatory mediators, and reduces the efficacy of the host response. Good controlled diabetes do not cause a major risk of periodontitis and improve the results of the periodontal therapy. Moreover periodontal therapy may reduce the request of insulin in diabetics. It is reasonable a two-ways relation between diabetes and periodontal disease.
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PMID:[Diabetes mellitus as a risk factor for periodontitis]. 1172 32

Interleukin-1 beta (IL-1beta) is a potent bone-resorptive cytokine that also mediates soft-tissue destruction by stimulating prostaglandin production and inducing collagenase and other protease activity. The literature suggests that this substance may be an important mediator of attachment loss in human periodontitis, and indicates that IL-1beta may be useful for locating sites of periodontal disease activity. There is some evidence that IL-1beta is produced by cells of the periodontium, and that it can be detected in gingival crevicular fluid (GCF). Many factors are known to contribute to the destruction of periodontal tissue. One of the most important is immune deficiency in diabetes. The aim of this study was to measure and compare the concentration of IL-1beta in the GCF of patients with non-insulin-dependent diabetes mellitus (Type 2 DM), otherwise healthy adults with periodontitis, and individuals with no periodontal disease in order to assess whether diabetes alters IL-1beta levels. We also examined relationships between GCF levels and the clinical parameters of pocket depth, plaque index, and bleeding index in each group. Seventeen patients with Type 2 DM, 17 adult periodontitis patients (AP), and 17 healthy controls were selected. The levels of IL-1beta in the GCF were quantified by ELISA. The mean IL-1beta concentrations in the Type 2 DM, AP, and control groups were 200.1 +/- 65.34 pg/microl, 131.35 +/- 67.66 pg/microl, and 80.0 +/- 36.08 pg/microl, respectively. The levels in the diabetic patients were significantly higher than those in the AP and control subjects. There were no significant correlations between IL-1beta level and any of the clinical data parameters for each group. We believe that the macrophages may over produce IL-beta in Type 2 DM and increased IL-1beta levels in diabetic patients could be linked to altered immune function.
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PMID:Interleukin-1 beta levels in gingival crevicular fluid in type 2 diabetes mellitus and adult periodontitis. 1173 37

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.
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PMID:Periodontitis and diabetes interrelationships: role of inflammation. 1188 55

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions.
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PMID:Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research. 1188 56

Diabetes mellitus, caused by the malfunction of insulin-dependent glucose and lipid metabolism, presents with the classical triad of symptoms: polydypsia, polyuria, and polyphagia which are often accompanied by chronic fatigue and loss of weight. Complications of diabetes mellitus include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Periodontal diseases are infections affecting the periodontium and resulting in the loss of tooth support. The association between diabetes mellitus and periodontitis has long been discussed with conflicting conclusions. Both of these diseases have a relatively high incidence in the general population (diabetes 1% to 6% and periodontitis 14%) as well as a number of common pathways in their pathogenesis (both diseases are polygenic disorders with some degree of immunoregulatory dysfunction). On the one hand, numerous reports indicate a higher incidence of periodontitis in diabetics compared to healthy controls, while other reports fail to show such a relationship. Clarification of this dilemma is occurring as the diagnostic criteria for periodontitis and diabetes mellitus improve, controlled studies with increased sample sizes are carried out, and the studies take into account major confounding variables that impact on the pathogenesis of both diseases. Current studies tend to support a higher incidence and severity of periodontitis in patients with diabetes mellitus. The overview looks at the bidirectional relationship between periodontitis and diabetes. An analysis of the National Health and Nutrition Examination Survey (NHANES) III data set confirms the previously reported significantly higher prevalence of periodontitis in diabetics than in non-diabetics (17.3% versus 9%). The analysis of the data also shows that the prevalence of diabetes in patients with periodontitis is double that seen in the non-periodontitis patients (12.5% versus 6.3%) and that this difference is also statistically significant. The pathogenesis of the 2 diseases is reviewed with an emphasis on common genetic and immune mechanisms. On the basis of the overview, 2 hypotheses for testing the relationship between periodontitis and diabetes are discussed. The first proposes a direct causal or modifying relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria-induced inflammatory periodontitis. The second hypothesis proposes that a fortuitous combination of genes (gene sets) could result in a host who, under the influence of a variety of environmental stressors, could develop either periodontitis or diabetes or both.
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PMID:The relationship between periodontal diseases and diabetes: an overview. 1188 77

This review evaluates evidence for a bidirectional relationship between diabetes and periodontal diseases. A comprehensive Medline search of the post-1960 English language literature was employed to identify primary research reports of relationships between diabetes and periodontal diseases. Reports included in the review on the adverse effects of diabetes on periodontal health (DM-->PD) were restricted to those comparing periodontal health in subjects with and without diabetes. Review of adverse affects of periodontal infection on glycemic control included reports of periodontal treatment studies and follow-up observational studies in which changes in glycemic control could be assessed. Observational studies reporting DM-->PD provided consistent evidence of greater prevalence, severity, extent, or progression of at least one manifestation of periodontal diseases in the large majority of reports (supportive evidence in 44/48 total reviewed; 37/41 cross-sectional and 7/7 cohort). Additionally, there were no studies reviewed with superior design features to refute this association. Treatment studies provided direct evidence to support periodontal infection having an adverse, yet modifiable, effect on glycemic control. However, not all investigations reported an improvement in glycemic control after periodontal treatment. Additional evidence to support the effect of severe periodontitis on increased risk for poorer glycemic control comes from 2 follow-up observational studies. The evidence reviewed supports viewing the relationship between diabetes and periodontal diseases as bidirectional. Further rigorous, systematic study is warranted to establish that treating periodontal infections can be influential in contributing to glycemic control management and possibly to the reduction of the burden of complications of diabetes mellitus.
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PMID:Bidirectional interrelationships between diabetes and periodontal diseases: an epidemiologic perspective. 1188 78

There is good evidence to support the claim that periodontitis may be more prevalent among diabetic patients than nondiabetic people. Similarly, studies have shown that periodontal therapy influences glycemic control in people with diabetes mellitus. Given that nearly 10% of Canadians are affected by either type 1 or type 2 diabetes (including those in whom the disease is undiagnosed), all dentists will encounter patients with diabetes. Dental practitioners must be aware of the implications of this relationship and manage their patients' periodontal care accordingly.
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PMID:The relationship between diabetes and periodontal disease. 1191 11

Retention of teeth into advanced age makes caries and periodontitis lifelong concerns. Dental caries occurs when acidic metabolites of oral streptococci dissolve enamel and dentin. Dissolution progresses to cavitation and, if untreated, to bacterial invasion of dental pulp, whereby oral bacteria access the bloodstream. Oral organisms have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Periodontitis is a pathogen-specific, lytic inflammatory reaction to dental plaque that degrades the tooth attachment. Periodontal disease is more severe and less readily controlled in people with diabetes; impaired glycemic control may exacerbate host response. Aspiration of oropharyngeal (including periodontal) pathogens is the dominant cause of nursing home-acquired pneumonia; factors reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne periodontopathic organisms may play a role in atherosclerosis. Daily oral hygiene practice and receipt of regular dental care are cost-effective means for minimizing morbidity of oral infections and their nonoral sequelae.
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PMID:Infectious complications of dental and periodontal diseases in the elderly population. 1295 53

Glucose quantification in serum or plasma is traditionally based on a colourimetric enzymatic assay using commercially available assay kits. Sample volumes of blood or serum are usually in the range of a few microlitres to a few millilitres. However, for biological fluids such as gingival crevicular fluid (GCF), which can only be sampled in submicrolitre volumes, such assays have proven unsuitable. The aim of this study was to develop a reliable and reproducible assay for quantifying glucose in submicrolitre samples of GCF. The assay involved modification of a commercially available kit for glucose quantification. Test solutions of (i) serum and (ii) serum with added glucose at known concentrations (range 50-400 mg/dl) were prepared to simulate GCF and GCF enriched with glucose, respectively. Submicrolitre volumes (range 0.2 microl to 0.8 microl) of the test solutions were added to the reagent solution (200 microl) using a Hamilton syringe. The reaction was performed under standard conditions of time and temperature. The colour change was assayed spectrophotometrically at 492 nm. The results showed that this microassay is sufficiently sensitive to detect 50 mg/dl glucose in 0.2 microl of sample and indicate that the accuracy and sensitivity of this assay make it suitable for glucose quantification in submicrolitre volumes of GCF, particularly relevant to investigations of the relationship between diabetes mellitus and chronic inflammatory periodontal disease. In vivo evaluation of this novel microassay was performed using GCF samples taken from periodontally healthy and chronic periodontitis patients. Using non-parametric analysis, the results showed that the assay detected statistically significant differences in glucose concentrations between the two patient groups (p < 0.05). Higher glucose levels were detected at the periodontally diseased sites. For each patient, the GCF-glucose: blood-glucose ratio was calculated. The results show that this ratio was higher in the periodontitis group (1: 2) when compared to the healthy group (1: 9). In conclusion, the results of this investigation have shown that this microassay can quantify glucose in GCF and that GCF-glucose levels are higher at periodontitis sites.
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PMID:Development of an in vitro microassay for glucose quantification in submicrolitre volumes of biological fluid. 1200 87


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