Association between dental factors and mortality

Peer reviewe

Salivary IgA antibody to malondialdehyde-acetaldehyde associates with mild periodontal pocket depth

Objective Oxidized epitopes such as malondialdehyde-acetaldehyde (MAA) play a crucial role in the progression of atherosclerosis through activation of the humoral immune response. The exact mechanism of the association between atherosclerosis and periodontal diseases is not fully understood. The aim of the current study is to evaluate the association of oral humoral immune response to oxidized epitopes with parameters of periodontal disease. Materials and methods The Parogene cohort consist of patients who have undergone coronary angiography due to cardiac symptoms. In this study, 423 patients were randomly selected for an extensive oral examination. Salivary Immunoglobulin A to oxidized epitopes and bacterial antigens was determined by chemiluminescence immunoassay. Results In a binary logistic regression model adjusted with periodontal disease confounders, periodontal pocket depth (PPD) 4-5 mm associated with salivary IgA antibodies to MAA-LDL (p = 0.034), heat shock protein 60 of Aggregatibacter actinomycetemcomitans (p = 0.045), Porphyromonas gingivalis (p = 0.045), A. actinomycetemcomitans (p = 0.005), P. intermedia (p = 0.020), and total IgA (p = 0.003). Conclusions The current study shows the association of salivary IgA to MAA-LDL with PPD 4-5 mm in a cohort of patients with chronic coronary artery disease. Humoral immune cross-reactivation to oxidized epitopes such MAA-LDL could partly explain the link of periodontitis with systemic diseases.Peer reviewe

Salivary IgA to MAA-LDL and Oral Pathogens Are Linked to Coronary Disease

A large body of literature has established the link between periodontal disease and cardiovascular disease. Oxidized low-density lipoproteins (OxLDLs) have a crucial role in atherosclerosis progression through initiation of immunological response. Monoclonal IgM antibodies to malondialdehyde-modified low-density lipoprotein (MDA-LDL) and to malondialdehyde acetaldehyde-modified low-density lipoprotein (MAA-LDL) have been shown to cross-react with the key virulence factors of periodontal pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. We have previously shown that salivary IgA antibodies to MAA-LDL cross-react with P. gingivalis in healthy humans. In this study, we aim to assess whether oral mucosal immune response represented by salivary IgA to MAA-LDL and oral pathogens is associated with coronary artery disease (CAD). Also, the molecular mimicry through antibody cross-reaction between salivary IgA to MAA-LDL and oral pathogens was evaluated. The study subjects consisted of 451 patients who underwent a coronary angiography with no CAD (n = 133), stable CAD (n = 169), and acute coronary syndrome (ACS, n = 149). Elevated salivary IgA antibody levels to MAA-LDL, Rgp44 (gingipain A hemagglutinin domain of P. gingivalis), and Aa-HSP60 (heat shock protein 60 of A. actinomycetemcomitans) were discovered in stable-CAD and ACS patients when compared to no-CAD patients. In a multinomial regression model adjusted for known cardiovascular risk factors, stable CAD and ACS were associated with IgA to MAA-LDL (P = 0.016, P = 0.043), Rgp44 (P = 0.012, P = 0.004), Aa-HSP60 (P = 0.032, P = 0.030), Tannerella forsythia (P = 0.002, P = 0.004), Porphyromonas endodontalis (P = 0.016, P = 0.020), Prevotella intermedia (P = 0.038, P = 0.005), and with total IgA antibody concentration (P = 0.002, P = 0.016). Salivary IgA to MAA-LDL showed cross-reactivity with the oral pathogens tested in the study patients. The study highlights an association between salivary IgA to MAA-LDL and atherosclerosis. However, whether salivary IgA to MAA-LDL and the related oral humoral responses play a causal role in the development in the CAD should be elucidated in the future.Peer reviewe

Salivary IgA to MAA-LDL and Oral Pathogens Are Linked to Coronary Disease

A large body of literature has established the link between periodontal disease and cardiovascular disease. Oxidized low-density lipoproteins (OxLDLs) have a crucial role in atherosclerosis progression through initiation of immunological response. Monoclonal IgM antibodies to malondialdehyde-modified low-density lipoprotein (MDA-LDL) and to malondialdehyde acetaldehyde-modified low-density lipoprotein (MAA-LDL) have been shown to cross-react with the key virulence factors of periodontal pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. We have previously shown that salivary IgA antibodies to MAA-LDL cross-react with P. gingivalis in healthy humans. In this study, we aim to assess whether oral mucosal immune response represented by salivary IgA to MAA-LDL and oral pathogens is associated with coronary artery disease (CAD). Also, the molecular mimicry through antibody cross-reaction between salivary IgA to MAA-LDL and oral pathogens was evaluated. The study subjects consisted of 451 patients who underwent a coronary angiography with no CAD (n = 133), stable CAD (n = 169), and acute coronary syndrome (ACS, n = 149). Elevated salivary IgA antibody levels to MAA-LDL, Rgp44 (gingipain A hemagglutinin domain of P. gingivalis), and Aa-HSP60 (heat shock protein 60 of A. actinomycetemcomitans) were discovered in stable-CAD and ACS patients when compared to no-CAD patients. In a multinomial regression model adjusted for known cardiovascular risk factors, stable CAD and ACS were associated with IgA to MAA-LDL (P = 0.016, P = 0.043), Rgp44 (P = 0.012, P = 0.004), Aa-HSP60 (P = 0.032, P = 0.030), Tannerella forsythia (P = 0.002, P = 0.004), Porphyromonas endodontalis (P = 0.016, P = 0.020), Prevotella intermedia (P = 0.038, P = 0.005), and with total IgA antibody concentration (P = 0.002, P = 0.016). Salivary IgA to MAA-LDL showed cross-reactivity with the oral pathogens tested in the study patients. The study highlights an association between salivary IgA to MAA-LDL and atherosclerosis. However, whether salivary IgA to MAA-LDL and the related oral humoral responses play a causal role in the development in the CAD should be elucidated in the future.Peer reviewe

Immunological and Microbiological Profiling of Cumulative Risk Score for Periodontitis

The cumulative risk score (CRS) is a mathematical salivary diagnostic model to define an individual’s risk of having periodontitis. In order to further validate this salivary biomarker, we investigated how periodontal bacteria, lipopolysaccharide (LPS), and systemic and local host immune responses relate to CRS. Subgingival plaque, saliva, and serum samples collected from 445 individuals were used in the analyses. Plaque levels of 28 microbial species, especially those of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella intermedia, and Tannerella forsythia, and serum and salivary levels of IgA and IgG against these five species were determined. Additionally, LPS activity was measured. High CRS associated strongly with all IgA/IgG antibody and LPS levels in saliva, whereas in serum the associations were not that obvious. In the final logistic regression model, the best predictors of high CRS were saliva IgA burden against the five species (OR 7.04, 95% CI 2.25–22.0), IgG burden (3.79, 1.78–8.08), LPS (2.19, 1.38–3.47), and the sum of 17 subgingival Gram-negative species (6.19, 2.10–18.3). CRS is strongly associated with microbial biomarker species of periodontitis and salivary humoral immune responses against them

Immunological and Microbiological Profiling of Cumulative Risk Score for Periodontitis

The cumulative risk score (CRS) is a mathematical salivary diagnostic model to define an individual’s risk of having periodontitis. In order to further validate this salivary biomarker, we investigated how periodontal bacteria, lipopolysaccharide (LPS), and systemic and local host immune responses relate to CRS. Subgingival plaque, saliva, and serum samples collected from 445 individuals were used in the analyses. Plaque levels of 28 microbial species, especially those of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella intermedia, and Tannerella forsythia, and serum and salivary levels of IgA and IgG against these five species were determined. Additionally, LPS activity was measured. High CRS associated strongly with all IgA/IgG antibody and LPS levels in saliva, whereas in serum the associations were not that obvious. In the final logistic regression model, the best predictors of high CRS were saliva IgA burden against the five species (OR 7.04, 95% CI 2.25–22.0), IgG burden (3.79, 1.78–8.08), LPS (2.19, 1.38–3.47), and the sum of 17 subgingival Gram-negative species (6.19, 2.10–18.3). CRS is strongly associated with microbial biomarker species of periodontitis and salivary humoral immune responses against them

Quantitative PCR analysis of salivary pathogen burden in periodontitis

Peer reviewe

Relationship between soy and isoflavone intake and periodontal disease: The Freshmen in Dietetic Courses Study II

<p>Abstract</p> <p>Background</p> <p>Much research has shown that soy products inhibited various diseases. However, no published studies have examined the effects of consumption of soy and isoflavones on periodontal disease. The aim of this study was to investigate whether soy and isoflavone intake is associated with the prevalence of periodontal disease.</p> <p>Methods</p> <p>The subjects were 3956 Japanese female students, aged 18 to 22 years, who were taking a dietetic course. Periodontal disease was defined as present when a subject reported diagnosis of the disorder by a dentist. Information on dietary factors was collected using a validated diet history questionnaire. Logistic regression analysis was used to estimate the odds ratios and their confidence intervals of periodontal disease. Adjustment was made for cigarette smoking, toothbrushing frequency, region of residence, and body mass index.</p> <p>Results</p> <p>The prevalence of periodontal disease was 8.0%. Intake of total soy product and tofu was independently associated with a decreased prevalence of periodontal disease; multivariate odds ratios in comparison of the highest with the lowest quintile were 0.68 and 0.68, respectively (95% confidence intervals = 0.47–0.97 and 0.47–0.98, <it>P </it>for trend = 0.01 and 0.004, respectively). A significant inverse dose-response relationship between the intake of isoflavones and the prevalence of periodontal disease was observed, although the difference in the adjusted odds ratio between the extreme quintiles was of borderline significance (<it>P </it>for trend = 0.04). There were no measurable dose-response relationships between consumption of tofu products, fermented soybeans, boiled soybeans, miso, or miso soup and the prevalence of periodontal disease.</p> <p>Conclusion</p> <p>Our findings suggest that soy and isoflavone intake may decrease the likelihood of periodontal disease. Further investigations with objective measures for periodontal disease are needed to confirm our findings.</p

Statin use is associated with fewer periodontal lesions: A retrospective study

<p>Abstract</p> <p>Background</p> <p>Inflammatory processes are considered to participate in the development of cardiovascular disease (CVD). Statins have been used successfully in the prevention and treatment of coronary heart disease. Chronic periodontitis has been suggested to contribute to CVD. The aim of this study was to examine the association of statin use and clinical markers of chronic periodontitis.</p> <p>Methods</p> <p>Periodontal probing pocket depth (PPD) values were collected from dental records of 100 consecutive adult patients referred to a university dental clinic for treatment of advanced chronic periodontitis. A novel index, Periodontal Inflammatory Burden Index (PIBI), was derived from the PPD values to estimate systemic effects of periodontitis.</p> <p>Results</p> <p>Periodontitis patients taking statins had a 37% lower number of pathological periodontal pockets than those without statin medication (P = 0.00043). PIBI, which combines and unifies the data on PPD, was 40% smaller in statin using patients than in patients without statin (P = 0.00069). PIBI of subjects on simvastatin and atorvastatin both differed significantly from patients without statin and were on the same level. The subjects' number of teeth had no effect on the results</p> <p>Conclusion</p> <p>Patients on statin medication exhibit fewer signs of periodontal inflammatory injury than subjects without the statin regimen. PIBI provides a tool for monitoring inflammatory load of chronic periodontitis. The apparent beneficial effects of statins may in part be mediated by their pleiotropic anti-inflammatory effect on periodontal tissue.</p

Immunological and Microbiological Profiling of Cumulative Risk Score for Periodontitis

The cumulative risk score (CRS) is a mathematical salivary diagnostic model to define an individual's risk of having periodontitis. In order to further validate this salivary biomarker, we investigated how periodontal bacteria, lipopolysaccharide (LPS), and systemic and local host immune responses relate to CRS. Subgingival plaque, saliva, and serum samples collected from 445 individuals were used in the analyses. Plaque levels of 28 microbial species, especially those ofAggregatibacter actinomycetemcomitans,Porphyromonas gingivalis,Porphyromonas endodontalis,Prevotella intermedia, andTannerella forsythia, and serum and salivary levels of IgA and IgG against these five species were determined. Additionally, LPS activity was measured. High CRS associated strongly with all IgA/IgG antibody and LPS levels in saliva, whereas in serum the associations were not that obvious. In the final logistic regression model, the best predictors of high CRS were saliva IgA burden against the five species (OR 7.04, 95% CI 2.25-22.0), IgG burden (3.79, 1.78-8.08), LPS (2.19, 1.38-3.47), and the sum of 17 subgingival Gram-negative species (6.19, 2.10-18.3). CRS is strongly associated with microbial biomarker species of periodontitis and salivary humoral immune responses against them