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At least 109 records · Page 6Linked to original sources
PubMed2006

Angiographically confirmed coronary heart disease and periodontal disease in middle-aged males.

BACKGROUND: The aim of this study was to investigate whether an association could be demonstrated between coronary heart disease (CHD) and chronic periodontitis in a population of middle-aged males in Northern Ireland. METHODS: A case-control design was used. Cases were men aged over 40 years with angiographically proven CHD. Controls were age-matched males, with no evidence of CHD, randomly drawn from the same locality as the cases. Each subject had a clinical periodontal examination and completed a detailed sociodemographic questionnaire. High sensitivity C-reactive protein (CRP) was measured in serum by immunoturbidimetry. RESULTS: There were 92 cases (mean age 56.7 years; SD = 6.3) and 79 controls (mean age 58.2 years; SD = 6.7). The CHD cases had an average of three teeth less than the controls (P <0.0001). A higher proportion of sites examined in cases than controls had plaque (P = 0.004), bleeding on probing (P = 0.013), and probing depths of > or = 4 mm (P = 0.006) or > or = 6 mm (P = 0.03). Subjects with > or = 4 mm pocketing in more than 20% of their interproximal sites and those with deep pocketing (> or = 6 mm) were classified as having poor periodontal status. A total of 35 cases (38%), compared to only 13 controls (16%), had a poor periodontal status (P = 0.0017). Men with a poor periodontal condition had higher levels of CRP (median 2.19 mg/l) than those with good periodontal health (median 1.42 mg/l), P = 0.007. After adjusting for smoking, academic achievement, alcohol consumption, unemployment, ability to maintain body weight, regular exercise, ability to relax daily, having a hobby or pastime, plaque, and CRP, logistic regression analysis showed that poor periodontal status was significantly associated with CHD, with an adjusted odds ratio of 3.06 and 95% confidence intervals of 1.02 to 9.17, P = 0.046. CONCLUSIONS: There was an association between coronary heart disease and poor periodontal status in the middle-aged males investigated. This association was independent of diabetes and all other cardiovascular risk factors investigated.

Adult↗
PubMedDate not supplied

Inflammation, cardiovascular disease and destructive periodontal diseases. The evolving role of the dental profession.

Destructive periodontal diseases have been associated with increased risk of atherosclerotic complications, including myocardial infarction (MI) and stroke. This finding comes at a time when our understanding of atherosclerotic complications are changing from a focus on the occlusion of arteries, due to the buildup of plaque deposits, to an increased awareness of the role of inflammation in plaque rupture and thrombus formation. The role of inflammation can have great significance to the dental profession if inflammatory cells and factors derived from chronic infections, such as destructive periodontal diseases, are shown to contribute to plaque rupture. This "Perspectives" feature will review the role of inflammation in atherosclerotic complications, and the association between destructive periodontal diseases, systemic inflammation and atherosclerotic complications. It will also highlight ongoing research designed to determine whether destructive periodontal diseases contribute to atherosclerotic complications.

Acute-Phase Reaction↗
PubMed1986

Design of clinical trials for chronic diseases: implications for periodontal disease.

In order to make effective use of the statistical theory of design of clinical trials for chronic diseases such as periodontal disease, certain issues must be considered. Any clinical trial requires that the disease definition be well-specified; that patient eligibility be explicit; that the observation times be explicit; that the duration and endpoint of therapy be specified; that the duration of subsequent followup observation be specified; and that the unit of observation (e.g., tooth, set of teeth, patient) be defined. In a chronic disease, the potential biases that can readily be introduced by self-selection of patients who enter the trial and/or who return for subsequent observation become more important, because subjects are required to remain on treatment and/or observation for prolonged periods. Further, the cyclical nature of some chronic diseases may require special attention to baseline definitions of active disease and disease outcome. These issues are illustrated with examples from clinical trials of hypertension, breast cancer screening, and Polycythemia Vera. Implications for periodontal disease are discussed.

Breast Neoplasms↗
PubMed1996

[Evaluation of the biosynthesis of mono-HETES and leukotrienes in diseased periodontal tissues].

Many arachidonic metabolites have been shown to have marked potent biological effects in animals. The cyclooxygenase and lipoxygenase products of arachidonate metabolism are known to play a key role in the development of inflammatory symptoms and signs. Reports published during past decades indicate that cyclooxygenase products of arachidonic acid metabolism are present in much higher concentrations in inflamed than in healthy periodontal tissues. Since information about the role of lipoxygenase products of arachidonic acid metabolism in human periodontal disease is lacking, the objective of this study was to determine the ability of diseased and non-diseased gingival tissue to synthesize lipoxygenase products from the precursor arachidonic acid. Twenty-six samples of diseased tissue and nine samples of non-diseased tissue were included in our data analysis. After incubation of the tissue with 100,000 cpm [3H]-arachidonic acid, lipoxygenase products were separated by high performance liquid chromatography (HPLC) and identified by comparison with cochromatographed standards. Our results showed that inflamed gingival tissue synthesized significantly larger amounts, of LTB4(p < 0.01), LTC4(p < 0.01), LTD4(p < 0.01), LTE4(p < 0.01), 5-HETE(p < 0.05), 12-HETE(p < 0.01), and 15-HETE(p < 0.01), compared to non-diseased tissue. The lipoxygenases are more active in inflamed gingival tissue than in non-diseased gingival tissue. 12-HETE and 15-HETE were the the major metabolites formed by lipoxygenases in diseased and non-diseased human gingiva. Since we did not functionally determine the fractions separated by HPLC, our present data may only provided indirect evidence for the existence of lipoxygenase products in periodontal tissue. However, our study did establish a research model for the investigation of arachidonic acid metabolism in the pathogenesis of periodontal disease.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2001

On the association between hypercholesterolemia, cardiovascular disease and severe periodontal disease.

BACKGROUND: Premature death in men is known to be significantly associated with coronary heart disease (CHD). More and more studies are pointing toward a possible association between periodontal disease and increased risk of cardiovascular disease. The association of poor oral hygiene and atherosclerosis can be explained by the effect of chronic inflammatory disease on blood rheology. The purpose of the present study was to assess the relationship between CHD and periodontal disease. PATIENTS AND METHODS: The study population included 1094 Israeli army service men aged 26-53 years (mean: 39+/-5 years). The study group comprised 151 subjects classified as having coronary heart disease CHD, i.e., myocardial infarction, and or anginal syndrome with angiographic evidence of significant coronary disease, or suffer from atherosclerotic risk factors, i.e., diabetes (fasting glucose) and HTN according to strict, well-established criteria. Blood levels of cholesterol and triglycerides were also determined. The severity of periodontal disease was assessed by the aid of CPITN. The control group comprised 943 healthy subjects. Statistical analysis was performed with chi2 test. RESULTS: Statistical analysis showed a significant association of CPITN score 4 with hypercholesterolemia and a possible association with CHD. CONCLUSIONS: The generation of higher cholesterol blood levels is proposed as a possible link between chronic periodontal inflammation and atherosclerosis.

Adult↗
PubMed2006

The use of different measurements and definitions of periodontal disease in the study of the association between periodontal disease and risk of myocardial infarction.

BACKGROUND: The role of periodontal disease as an independent risk factor for cardiovascular disease (CVD) has been under debate because of the inconsistency of findings across studies. One of the major issues is the method used to assess or define periodontal disease. The present study assesses if the observed association between periodontal disease and incident myocardial infarction (MI) depends on the measurements and/or criteria used to define periodontal disease. METHODS: A population-based case-control study to evaluate the association between PD and risk of MI was conducted between 1997 and 2001 in Western New York with 537 cases and 800 controls, aged 35 to 69 years. Cases were survivors of incident MI from local hospitals in Erie and Niagara counties. Controls were randomly selected from residents of the same counties. Periodontal disease was assessed using interproximal clinical attachment loss (CAL), probing depth (PD), alveolar crest height (ACH), and number of missing teeth. From these measurements, four different case definitions of periodontal disease were created. RESULTS: Using the continuous forms of periodontal measurements, the odds ratios (ORs) (95% confidence interval) of the association with incident MI were 1.46 (1.26 to 1.69), 2.19 (1.66 to 2.89), 1.30 (1.14 to 1.49), and 1.04 (1.02 to 1.07) for mean CAL, PD, ACH, and number of missing teeth, respectively. Regardless of the case definition of periodontal disease, the estimates of the association with incident MI were statistically significant. CONCLUSIONS: The observed association between periodontal disease and incident MI was consistent across different measurements and/or case definitions of periodontal disease used. The magnitude of the association varies depending on the measurements or the criteria used to define periodontal disease.

Adult↗
PubMed1991

The normal and diseased periodontium and periodontal disease activity.

Scientific knowledge regarding the cellular and molecular biology of the periodontium in health is fundamental to the determination of how periodontal diseases begin and progress. Advances in diagnosis and treatment are in turn becoming increasingly dependent upon advances in the molecular biology of inflammation-induced changes in the periodontal tissues, and the regenerative capacity of the periodontal cells. New in vitro cell culture models, a broadening array of monoclonal antibody reagents, and general advances in scientific methodology have presented the field of periodontal research with excellent opportunities to explore the mechanisms of tissue destruction, as well as test innovative means to induce tissue regeneration. Laboratory and clinical findings in the past year have led to major expansions in how we perceive the pathogenesis of periodontal diseases, and also have altered our long-held beliefs about periodontal disease activity.

Alveolar Bone Loss↗
PubMed2001

The relationship between periodontal diseases and diabetes: an overview.

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.

Diabetes Complications↗
PubMed1999

Destructive membranous periodontal disease (Ligneous periodontitis).

Generalized membranous gingival enlargement due to accumulation of amyloid or fibrin-like material is a rare, destructive and poorly defined disease entity. Some patients also show extraoral manifestations. The lesion is an involvement of periodontal tissues caused by the same process as ligneous conjunctivitis. In this report, 3 new cases, two of whom are siblings, are presented. Defective fibrinolysis and abnormal wound healing seem to be the main pathogenetic mechanism of this unusual disease, which should be evaluated systemically considering other mucosal involvement.

Adolescent↗