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David R Jacobs - One of the best experts on this subject based on the ideXlab platform.
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Periodontal infection and cardiorespiratory fitness in younger adults results from continuous national health and nutrition Examination survey 1999 2004
PLOS ONE, 2014Co-Authors: Ashley Thai, Panos N Papapanou, David R Jacobs, Moise Desvarieu, Rya T DemmeAbstract:OBJECTIVE Previous studies report associations between Periodontal infection and cardiorespiratory fitness but no study has examined the association among younger adults. Our objective was to study the association between clinical measures of Periodontal infection and cardiorespiratory fitness levels among a population-based sample of younger adults. METHODS The Continuous National Health and Nutrition Examination Survey 1999-2004 enrolled 2,863 participants (46% women) who received a partial-mouth Periodontal Examination and completed a submaximal treadmill test for the assessment of estimated VO2 max(eVO2 max ). Participants were mean±SD age 33±9 years (range = 20-49 years), 30% Hispanic, 48% White, 19% Black, and 3% other. Mean eVO2 max (mL/kg/minute) as well as eVO2 max≤32 mL/kg/minute (20th percentile) were regressed across quartiles of mean probing depth and mean attachment loss in multivariable linear and logistic regression models. RESULTS After multivariable adjustment, mean eVO2 max levels±SE across quartiles of attachment loss were 39.72±0.37, 39.64±0.34, 39.59±0.36, and 39.85±0.39 (P = 0.99). Mean eVO2 max±SE across quartiles of probing depth were 39.57±0.32, 39.78±0.38, 39.19±0.25, and 40.37±0.53 (P = 0.28). Similarly, multivariable adjusted mean eVO2 max values were similar between healthy participants vs. those with moderate/severe periodontitis: 39.70±0.21 vs. 39.70±0.90 (P = 1.00). The odds ratio (OR) for low eVO2 max comparing highest vs. lowest quartile of attachment loss = 0.89[95% CI 0.64-1.24]. The OR for comparing highest vs. lowest probing depth quartile = 0.77[95% CI 0.51-1.15]. CONCLUSION Clinical measures of Periodontal infection were not related to cardiorespiratory fitness in a sample of generally healthy younger adults.
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Periodontal infection systemic inflammation and insulin resistance results from the continuous national health and nutrition Examination survey nhanes 1999 2004
Diabetes Care, 2012Co-Authors: Rya T Demme, Panos N Papapanou, David R Jacobs, Anthony I Squillaro, Michael Rosenbaum, William T Friedewald, Moise DesvarieuAbstract:OBJECTIVE Adverse microbial exposures might contribute to diabetogenesis. We hypothesized that clinical Periodontal disease (a manifestation of microbial exposures in dysbiotic biofilms) would be related to insulin resistance among diabetes-free participants. The roles of inflammatory mediation and effect modification were also studied. RESEARCH DESIGN AND METHODS The continuous National Health and Nutrition Examination Survey 1999–2004 enrolled 3,616 participants (51% women) who received a Periodontal Examination and fasting blood draw. Participants were mean age (± SD) 43 ± 17 years and 28% Hispanic, 52% Caucasian, 17% African American, and 3% other. Log-transformed values of the homeostasis model assessment of insulin resistance (HOMA-IR) or HOMA-IR ≥3.30 (75th percentile) were regressed across full-mouth Periodontal probing depth (PD) levels using linear and logistic models. White blood cell (WBC) count and C-reactive protein (CRP) were considered as either mediators or effect modifiers in separate analyses. Risk ratios (RRs) stem from marginal predictions derived from the logistic model. Results were adjusted for multiple Periodontal disease and insulin resistance risk factors. RESULTS In linear regression, geometric mean HOMA-IR levels increased by 1.04 for every 1-mm PD increase ( P = 0.007). WBC mediated 6% of the association ( P 9 , PD was unrelated to HOMA-IR ≥3.30. Fourth-quartile PD was associated with HOMA-IR ≥3.30 among participants with WBC >7.9 × 10 9 ; RR 2.60 (1.36–4.97) ( P for interaction = 0.05). Findings were similar among participants with CRP >3.0 mg/L ( P for interaction = 0.04). CONCLUSIONS Periodontal infection was associated with insulin resistance in a nationally representative U.S. sample of diabetes-free adults. These data support the role of inflammation as both mediator and effect modifier of the association.
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Periodontal disease tooth loss and incident rheumatoid arthritis results from the first national health and nutrition Examination survey and its epidemiological follow up study
Journal of Clinical Periodontology, 2011Co-Authors: Rya T Demme, David R Jacobs, Jerry A Molito, Ya S MichalowiczAbstract:Rheumatoid Arthritis (RA) is a chronic, disabling disease affecting 0.5–1% of the population(Tobon et al., 2010). Early and aggressive interventions have reduced the rate of progression of the disease and its long-term disability(Klareskog et al., 2009). Nevertheless, the majority of patients continue to require lifelong, often expensive or inaccessible therapy, and have increased mortality, particularly due to cardiovascular disease even with more aggressive and modern treatments(Gabriel, 2008). Thus, there is a strong need to understand the risk factors and preclinical disease pathways leading to clinical RA, to facilitate preclinical RA intervention. The most important known risk factors for RA are genetic. The “shared epitope” (SE) – a short peptide sequence found in multiple HLA-DR alleles – is the most significant genetic risk factor, and cigarette smoking interacts with SE alleles to increase the risk for autoantibodies against citrullinated peptides that predict risk for RA(Klareskog et al., 2009). Microbial exposures have been suggested as a risk factor for RA(Rosenstein et al., 2004). Periodontal disease, which is partly caused by gram-negative anaerobic bacterial species(Haffajee and Socransky, 1994, Papapanou et al., 1997, Timmerman et al., 2001, van Winkelhoff et al., 2002, Van der Velden et al., 2006, Paster et al., 2006, Demmer et al., 2008c), shares several pathobiological features with RA(Rosenstein et al., 2004, Culshaw et al., 2011). Two recent small clinical trials have demonstrated that Periodontal therapy among RA patients can reduce RA disease activity(Al-Katma et al., 2007, Ortiz et al., 2009) providing evidence that Periodontal infections might exacerbate RA severity. Others have reported associations between periodontitis and RA in cross-sectional studies(de Pablo et al., 2008, Pischon et al., 2008, de Pablo et al., 2009). Such associations, however, may arise from shared environmental or genetic risk factors that result in similar pathobiology. Importantly, associations between periodontitis and RA have been observed following adjustment for smoking, which is the most important known shared environmental risk factor(de Pablo et al., 2008, de Pablo et al., 2009, Molitor, 2009). Thus, Periodontal disease pathobiology might contribute to the development of RA or vice versa. Longitudinal analyses can help to establish the temporal relationship between clinical Periodontal disease and RA. The only available longitudinal data that followed the development of RA subsequent to the assessment of Periodontal infection suggest increased incidence of RA in never smokers with moderate to severe periodontitis in the Atherosclerosis Risk in Communities (ARIC) cohort(Molitor, 2009). The First National Health and Nutrition Examination Survey (NHANES I) and its epidemiological follow – up study (NHEFS) provide a unique opportunity to examine the association between prevalent Periodontal disease and both prevalent and incident RA because: i) both medical and dental evaluations were conducted concurrently at baseline; and ii) the large nationally representative sample and long longitudinal follow-up period enabled the accumulation of adequate RA event rates. We tested the hypothesis that baseline evidence of historical exposure to Periodontal infections (assessed via clinical Periodontal Examination and tooth loss status) can predict both prevalent and incident RA in the nationally representative, population-based setting of NHANES I and NHEFS. Based on findings from the ARIC study(Molitor, 2009), we also hypothesized that the association with incident RA would be strongest in never smokers. We have included the cross-sectional aims in our current report to establish consistency with previous research.
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relationship between Periodontal disease tooth loss and carotid artery plaque the oral infections and vascular disease epidemiology study invest
Stroke, 2003Co-Authors: Moise Desvarieux, Panos N Papapanou, Ryan T Demmer, Tatjana Rundek, Bernadette Bodenalbala, David R Jacobs, Ralph L SaccoAbstract:Background and Purpose—Chronic infections, including Periodontal infections, may predispose to cardiovascular disease. The present study investigates the relationship of Periodontal disease and tooth loss with subclinical atherosclerosis. Methods—We enrolled 711 subjects with a mean age of 669 years and no history of stroke or myocardial infarction in the Oral Infections and Vascular Disease Epidemiology Study. Subjects received a comprehensive Periodontal Examination, extensive in-person cardiovascular disease risk factor measurements, and a carotid scan using highresolution B-mode ultrasound. Regression models were adjusted for conventional risk factors (age, sex, smoking, diabetes, systolic blood pressure, low- and high-density lipoprotein cholesterol, race-ethnicity, education, physical activity) and markers of cultural background, healthy lifestyle, and psychosocial health. Results—Measures of both current and cumulative periodontitis became more severe as tooth loss increased. A significant association was observed between tooth loss levels and carotid artery plaque prevalence. Among those with 0 to 9 missing teeth, 46% had carotid artery plaque, whereas among those with 10 missing teeth, carotid artery plaque prevalence was 60% (P0.05). Conclusions—Our data suggest that tooth loss is a marker of past Periodontal disease in this population and is related to subclinical atherosclerosis, thereby providing a potential pathway for a relationship with clinical events. (Stroke. 2003; 34:2120-2125.)
Rya T Demme - One of the best experts on this subject based on the ideXlab platform.
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association between low dose aspirin and Periodontal disease results from the continuous national health and nutrition Examination survey nhanes 2011 2012
Journal of Clinical Periodontology, 2015Co-Authors: Georgios A Kotsakis, Ashley Thai, Andreas L Ioannou, Rya T Demme, Ya S MichalowiczAbstract:AIM Low-dose aspirin has been hypothesized as being a potential host modulatory agent for periodontitis treatment. We investigated the relationship between low-dose aspirin use and periodontitis prevalence in the continuous National Health and Nutrition Examination Survey, 2011-2012. METHODS We analysed n = 2335 adult men and women who received a full-mouth Periodontal Examination and responded to an aspirin use questionnaire. Periodontal disease was defined as severe, moderate or mild according to established case definitions. Mean full-mouth probing depth, attachment loss and tooth loss were also considered. Low-dose aspirin was defined by any self-reported, physician prescribed aspirin use of ≤162 mg/day. RESULTS Participants had mean age (SE) 55.8 years (0.42). The prevalences of periodontitis and low-dose aspirin use were 49.5% and 25% respectively. In multivariable logistic regression models controlling for age, sex, race, socioeconomic variables and comorbidities, the odds ratios [95%CI] for moderate or severe periodontitis among low-dose aspirin users (versus non-users) were: 0.91 [0.56-1.50] and 1.06 [0.74-1.50] respectively. Results were unchanged among participants without diabetes or coronary heart disease. CONCLUSIONS Within the limitations of this cross-sectional study we conclude that low-dose aspirin is not associated with prevalent Periodontal status in a nationally representative sample of US adults.
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Periodontal infection and cardiorespiratory fitness in younger adults results from continuous national health and nutrition Examination survey 1999 2004
PLOS ONE, 2014Co-Authors: Ashley Thai, Panos N Papapanou, David R Jacobs, Moise Desvarieu, Rya T DemmeAbstract:OBJECTIVE Previous studies report associations between Periodontal infection and cardiorespiratory fitness but no study has examined the association among younger adults. Our objective was to study the association between clinical measures of Periodontal infection and cardiorespiratory fitness levels among a population-based sample of younger adults. METHODS The Continuous National Health and Nutrition Examination Survey 1999-2004 enrolled 2,863 participants (46% women) who received a partial-mouth Periodontal Examination and completed a submaximal treadmill test for the assessment of estimated VO2 max(eVO2 max ). Participants were mean±SD age 33±9 years (range = 20-49 years), 30% Hispanic, 48% White, 19% Black, and 3% other. Mean eVO2 max (mL/kg/minute) as well as eVO2 max≤32 mL/kg/minute (20th percentile) were regressed across quartiles of mean probing depth and mean attachment loss in multivariable linear and logistic regression models. RESULTS After multivariable adjustment, mean eVO2 max levels±SE across quartiles of attachment loss were 39.72±0.37, 39.64±0.34, 39.59±0.36, and 39.85±0.39 (P = 0.99). Mean eVO2 max±SE across quartiles of probing depth were 39.57±0.32, 39.78±0.38, 39.19±0.25, and 40.37±0.53 (P = 0.28). Similarly, multivariable adjusted mean eVO2 max values were similar between healthy participants vs. those with moderate/severe periodontitis: 39.70±0.21 vs. 39.70±0.90 (P = 1.00). The odds ratio (OR) for low eVO2 max comparing highest vs. lowest quartile of attachment loss = 0.89[95% CI 0.64-1.24]. The OR for comparing highest vs. lowest probing depth quartile = 0.77[95% CI 0.51-1.15]. CONCLUSION Clinical measures of Periodontal infection were not related to cardiorespiratory fitness in a sample of generally healthy younger adults.
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Periodontal infection systemic inflammation and insulin resistance results from the continuous national health and nutrition Examination survey nhanes 1999 2004
Diabetes Care, 2012Co-Authors: Rya T Demme, Panos N Papapanou, David R Jacobs, Anthony I Squillaro, Michael Rosenbaum, William T Friedewald, Moise DesvarieuAbstract:OBJECTIVE Adverse microbial exposures might contribute to diabetogenesis. We hypothesized that clinical Periodontal disease (a manifestation of microbial exposures in dysbiotic biofilms) would be related to insulin resistance among diabetes-free participants. The roles of inflammatory mediation and effect modification were also studied. RESEARCH DESIGN AND METHODS The continuous National Health and Nutrition Examination Survey 1999–2004 enrolled 3,616 participants (51% women) who received a Periodontal Examination and fasting blood draw. Participants were mean age (± SD) 43 ± 17 years and 28% Hispanic, 52% Caucasian, 17% African American, and 3% other. Log-transformed values of the homeostasis model assessment of insulin resistance (HOMA-IR) or HOMA-IR ≥3.30 (75th percentile) were regressed across full-mouth Periodontal probing depth (PD) levels using linear and logistic models. White blood cell (WBC) count and C-reactive protein (CRP) were considered as either mediators or effect modifiers in separate analyses. Risk ratios (RRs) stem from marginal predictions derived from the logistic model. Results were adjusted for multiple Periodontal disease and insulin resistance risk factors. RESULTS In linear regression, geometric mean HOMA-IR levels increased by 1.04 for every 1-mm PD increase ( P = 0.007). WBC mediated 6% of the association ( P 9 , PD was unrelated to HOMA-IR ≥3.30. Fourth-quartile PD was associated with HOMA-IR ≥3.30 among participants with WBC >7.9 × 10 9 ; RR 2.60 (1.36–4.97) ( P for interaction = 0.05). Findings were similar among participants with CRP >3.0 mg/L ( P for interaction = 0.04). CONCLUSIONS Periodontal infection was associated with insulin resistance in a nationally representative U.S. sample of diabetes-free adults. These data support the role of inflammation as both mediator and effect modifier of the association.
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Periodontal disease tooth loss and incident rheumatoid arthritis results from the first national health and nutrition Examination survey and its epidemiological follow up study
Journal of Clinical Periodontology, 2011Co-Authors: Rya T Demme, David R Jacobs, Jerry A Molito, Ya S MichalowiczAbstract:Rheumatoid Arthritis (RA) is a chronic, disabling disease affecting 0.5–1% of the population(Tobon et al., 2010). Early and aggressive interventions have reduced the rate of progression of the disease and its long-term disability(Klareskog et al., 2009). Nevertheless, the majority of patients continue to require lifelong, often expensive or inaccessible therapy, and have increased mortality, particularly due to cardiovascular disease even with more aggressive and modern treatments(Gabriel, 2008). Thus, there is a strong need to understand the risk factors and preclinical disease pathways leading to clinical RA, to facilitate preclinical RA intervention. The most important known risk factors for RA are genetic. The “shared epitope” (SE) – a short peptide sequence found in multiple HLA-DR alleles – is the most significant genetic risk factor, and cigarette smoking interacts with SE alleles to increase the risk for autoantibodies against citrullinated peptides that predict risk for RA(Klareskog et al., 2009). Microbial exposures have been suggested as a risk factor for RA(Rosenstein et al., 2004). Periodontal disease, which is partly caused by gram-negative anaerobic bacterial species(Haffajee and Socransky, 1994, Papapanou et al., 1997, Timmerman et al., 2001, van Winkelhoff et al., 2002, Van der Velden et al., 2006, Paster et al., 2006, Demmer et al., 2008c), shares several pathobiological features with RA(Rosenstein et al., 2004, Culshaw et al., 2011). Two recent small clinical trials have demonstrated that Periodontal therapy among RA patients can reduce RA disease activity(Al-Katma et al., 2007, Ortiz et al., 2009) providing evidence that Periodontal infections might exacerbate RA severity. Others have reported associations between periodontitis and RA in cross-sectional studies(de Pablo et al., 2008, Pischon et al., 2008, de Pablo et al., 2009). Such associations, however, may arise from shared environmental or genetic risk factors that result in similar pathobiology. Importantly, associations between periodontitis and RA have been observed following adjustment for smoking, which is the most important known shared environmental risk factor(de Pablo et al., 2008, de Pablo et al., 2009, Molitor, 2009). Thus, Periodontal disease pathobiology might contribute to the development of RA or vice versa. Longitudinal analyses can help to establish the temporal relationship between clinical Periodontal disease and RA. The only available longitudinal data that followed the development of RA subsequent to the assessment of Periodontal infection suggest increased incidence of RA in never smokers with moderate to severe periodontitis in the Atherosclerosis Risk in Communities (ARIC) cohort(Molitor, 2009). The First National Health and Nutrition Examination Survey (NHANES I) and its epidemiological follow – up study (NHEFS) provide a unique opportunity to examine the association between prevalent Periodontal disease and both prevalent and incident RA because: i) both medical and dental evaluations were conducted concurrently at baseline; and ii) the large nationally representative sample and long longitudinal follow-up period enabled the accumulation of adequate RA event rates. We tested the hypothesis that baseline evidence of historical exposure to Periodontal infections (assessed via clinical Periodontal Examination and tooth loss status) can predict both prevalent and incident RA in the nationally representative, population-based setting of NHANES I and NHEFS. Based on findings from the ARIC study(Molitor, 2009), we also hypothesized that the association with incident RA would be strongest in never smokers. We have included the cross-sectional aims in our current report to establish consistency with previous research.
Panos N Papapanou - One of the best experts on this subject based on the ideXlab platform.
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standards for reporting chronic periodontitis prevalence and severity in epidemiologic studies proposed standards from the joint eu usa Periodontal epidemiology working group
Journal of Clinical Periodontology, 2015Co-Authors: Birte Holtfreter, Jasim M Albandar, Thomas Dietrich, Kenneth A Eaton, Panos N Papapanou, Thomas KocherAbstract:Periodontal diseases are common and their prevalence varies in different populations. However, prevalence estimates are influenced by the methodology used, including measurement techniques, case definitions, and Periodontal Examination protocols, as well as differences in oral health status. As a consequence, comparisons between populations are severely hampered and inferences regarding the global variation in prevalence can hardly be drawn. To overcome these limitations, the authors suggest standardized principles for the reporting of the prevalence and severity of Periodontal diseases in future epidemiological studies. These principles include the comprehensive reporting of the study design, the recording protocol, and specific subject-related and oral data. Further, a range of Periodontal data should be reported in the total population and within specific age groups. Periodontal data include the prevalence and extent of clinical attachment loss (CAL) and probing depth (PD) on site and tooth level according to specific thresholds, mean CAL/PD, the CDC/AAP case definition, and bleeding on probing. Consistent implementation of these standards in future studies will ensure improved reporting quality, permit meaningful comparisons of the prevalence of Periodontal diseases across populations, and provide better insights into the determinants of such variation.
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Periodontal infection and cardiorespiratory fitness in younger adults results from continuous national health and nutrition Examination survey 1999 2004
PLOS ONE, 2014Co-Authors: Ashley Thai, Panos N Papapanou, David R Jacobs, Moise Desvarieu, Rya T DemmeAbstract:OBJECTIVE Previous studies report associations between Periodontal infection and cardiorespiratory fitness but no study has examined the association among younger adults. Our objective was to study the association between clinical measures of Periodontal infection and cardiorespiratory fitness levels among a population-based sample of younger adults. METHODS The Continuous National Health and Nutrition Examination Survey 1999-2004 enrolled 2,863 participants (46% women) who received a partial-mouth Periodontal Examination and completed a submaximal treadmill test for the assessment of estimated VO2 max(eVO2 max ). Participants were mean±SD age 33±9 years (range = 20-49 years), 30% Hispanic, 48% White, 19% Black, and 3% other. Mean eVO2 max (mL/kg/minute) as well as eVO2 max≤32 mL/kg/minute (20th percentile) were regressed across quartiles of mean probing depth and mean attachment loss in multivariable linear and logistic regression models. RESULTS After multivariable adjustment, mean eVO2 max levels±SE across quartiles of attachment loss were 39.72±0.37, 39.64±0.34, 39.59±0.36, and 39.85±0.39 (P = 0.99). Mean eVO2 max±SE across quartiles of probing depth were 39.57±0.32, 39.78±0.38, 39.19±0.25, and 40.37±0.53 (P = 0.28). Similarly, multivariable adjusted mean eVO2 max values were similar between healthy participants vs. those with moderate/severe periodontitis: 39.70±0.21 vs. 39.70±0.90 (P = 1.00). The odds ratio (OR) for low eVO2 max comparing highest vs. lowest quartile of attachment loss = 0.89[95% CI 0.64-1.24]. The OR for comparing highest vs. lowest probing depth quartile = 0.77[95% CI 0.51-1.15]. CONCLUSION Clinical measures of Periodontal infection were not related to cardiorespiratory fitness in a sample of generally healthy younger adults.
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Periodontal infection systemic inflammation and insulin resistance results from the continuous national health and nutrition Examination survey nhanes 1999 2004
Diabetes Care, 2012Co-Authors: Rya T Demme, Panos N Papapanou, David R Jacobs, Anthony I Squillaro, Michael Rosenbaum, William T Friedewald, Moise DesvarieuAbstract:OBJECTIVE Adverse microbial exposures might contribute to diabetogenesis. We hypothesized that clinical Periodontal disease (a manifestation of microbial exposures in dysbiotic biofilms) would be related to insulin resistance among diabetes-free participants. The roles of inflammatory mediation and effect modification were also studied. RESEARCH DESIGN AND METHODS The continuous National Health and Nutrition Examination Survey 1999–2004 enrolled 3,616 participants (51% women) who received a Periodontal Examination and fasting blood draw. Participants were mean age (± SD) 43 ± 17 years and 28% Hispanic, 52% Caucasian, 17% African American, and 3% other. Log-transformed values of the homeostasis model assessment of insulin resistance (HOMA-IR) or HOMA-IR ≥3.30 (75th percentile) were regressed across full-mouth Periodontal probing depth (PD) levels using linear and logistic models. White blood cell (WBC) count and C-reactive protein (CRP) were considered as either mediators or effect modifiers in separate analyses. Risk ratios (RRs) stem from marginal predictions derived from the logistic model. Results were adjusted for multiple Periodontal disease and insulin resistance risk factors. RESULTS In linear regression, geometric mean HOMA-IR levels increased by 1.04 for every 1-mm PD increase ( P = 0.007). WBC mediated 6% of the association ( P 9 , PD was unrelated to HOMA-IR ≥3.30. Fourth-quartile PD was associated with HOMA-IR ≥3.30 among participants with WBC >7.9 × 10 9 ; RR 2.60 (1.36–4.97) ( P for interaction = 0.05). Findings were similar among participants with CRP >3.0 mg/L ( P for interaction = 0.04). CONCLUSIONS Periodontal infection was associated with insulin resistance in a nationally representative U.S. sample of diabetes-free adults. These data support the role of inflammation as both mediator and effect modifier of the association.
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relationship between Periodontal disease tooth loss and carotid artery plaque the oral infections and vascular disease epidemiology study invest
Stroke, 2003Co-Authors: Moise Desvarieux, Panos N Papapanou, Ryan T Demmer, Tatjana Rundek, Bernadette Bodenalbala, David R Jacobs, Ralph L SaccoAbstract:Background and Purpose—Chronic infections, including Periodontal infections, may predispose to cardiovascular disease. The present study investigates the relationship of Periodontal disease and tooth loss with subclinical atherosclerosis. Methods—We enrolled 711 subjects with a mean age of 669 years and no history of stroke or myocardial infarction in the Oral Infections and Vascular Disease Epidemiology Study. Subjects received a comprehensive Periodontal Examination, extensive in-person cardiovascular disease risk factor measurements, and a carotid scan using highresolution B-mode ultrasound. Regression models were adjusted for conventional risk factors (age, sex, smoking, diabetes, systolic blood pressure, low- and high-density lipoprotein cholesterol, race-ethnicity, education, physical activity) and markers of cultural background, healthy lifestyle, and psychosocial health. Results—Measures of both current and cumulative periodontitis became more severe as tooth loss increased. A significant association was observed between tooth loss levels and carotid artery plaque prevalence. Among those with 0 to 9 missing teeth, 46% had carotid artery plaque, whereas among those with 10 missing teeth, carotid artery plaque prevalence was 60% (P0.05). Conclusions—Our data suggest that tooth loss is a marker of past Periodontal disease in this population and is related to subclinical atherosclerosis, thereby providing a potential pathway for a relationship with clinical events. (Stroke. 2003; 34:2120-2125.)
D Bourgeois - One of the best experts on this subject based on the ideXlab platform.
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risk assessment for severe clinical attachment loss in an adult population
Journal of Periodontology, 2006Co-Authors: Philippe Bouchard, Pierre Boutouyrie, C Mattout, D BourgeoisAbstract:Background: This study was carried out to identify variables related to severe clinical attachment loss (CAL) in an adult French population.Methods: This cross-sectional survey employed 2,132 subjects of the First National Periodontal and Systemic Examination Survey (NPASES I) aged 35 to 64 years, each with at least six teeth. A nationally representative sample was obtained from September 2002 to June 2003 by a quota method stratified on age, gender, socioeconomic status, and geographic areas. The subjects had a complete full-mouth Periodontal Examination of four sites per tooth, assessment of missing teeth, and a number of laboratory tests and questionnaires. The Periodontal status of each subject was assessed by criteria based on the severity and extent of CAL. The data were analyzed by univariable and multivariable models using logistic regression analyses.Results: Nineteen and seven-tenths percent (19.7%) of the subjects had CAL >5 mm. When dental variables were not included in the analysis (model 1),...
Ya S Michalowicz - One of the best experts on this subject based on the ideXlab platform.
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association between low dose aspirin and Periodontal disease results from the continuous national health and nutrition Examination survey nhanes 2011 2012
Journal of Clinical Periodontology, 2015Co-Authors: Georgios A Kotsakis, Ashley Thai, Andreas L Ioannou, Rya T Demme, Ya S MichalowiczAbstract:AIM Low-dose aspirin has been hypothesized as being a potential host modulatory agent for periodontitis treatment. We investigated the relationship between low-dose aspirin use and periodontitis prevalence in the continuous National Health and Nutrition Examination Survey, 2011-2012. METHODS We analysed n = 2335 adult men and women who received a full-mouth Periodontal Examination and responded to an aspirin use questionnaire. Periodontal disease was defined as severe, moderate or mild according to established case definitions. Mean full-mouth probing depth, attachment loss and tooth loss were also considered. Low-dose aspirin was defined by any self-reported, physician prescribed aspirin use of ≤162 mg/day. RESULTS Participants had mean age (SE) 55.8 years (0.42). The prevalences of periodontitis and low-dose aspirin use were 49.5% and 25% respectively. In multivariable logistic regression models controlling for age, sex, race, socioeconomic variables and comorbidities, the odds ratios [95%CI] for moderate or severe periodontitis among low-dose aspirin users (versus non-users) were: 0.91 [0.56-1.50] and 1.06 [0.74-1.50] respectively. Results were unchanged among participants without diabetes or coronary heart disease. CONCLUSIONS Within the limitations of this cross-sectional study we conclude that low-dose aspirin is not associated with prevalent Periodontal status in a nationally representative sample of US adults.
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Periodontal disease tooth loss and incident rheumatoid arthritis results from the first national health and nutrition Examination survey and its epidemiological follow up study
Journal of Clinical Periodontology, 2011Co-Authors: Rya T Demme, David R Jacobs, Jerry A Molito, Ya S MichalowiczAbstract:Rheumatoid Arthritis (RA) is a chronic, disabling disease affecting 0.5–1% of the population(Tobon et al., 2010). Early and aggressive interventions have reduced the rate of progression of the disease and its long-term disability(Klareskog et al., 2009). Nevertheless, the majority of patients continue to require lifelong, often expensive or inaccessible therapy, and have increased mortality, particularly due to cardiovascular disease even with more aggressive and modern treatments(Gabriel, 2008). Thus, there is a strong need to understand the risk factors and preclinical disease pathways leading to clinical RA, to facilitate preclinical RA intervention. The most important known risk factors for RA are genetic. The “shared epitope” (SE) – a short peptide sequence found in multiple HLA-DR alleles – is the most significant genetic risk factor, and cigarette smoking interacts with SE alleles to increase the risk for autoantibodies against citrullinated peptides that predict risk for RA(Klareskog et al., 2009). Microbial exposures have been suggested as a risk factor for RA(Rosenstein et al., 2004). Periodontal disease, which is partly caused by gram-negative anaerobic bacterial species(Haffajee and Socransky, 1994, Papapanou et al., 1997, Timmerman et al., 2001, van Winkelhoff et al., 2002, Van der Velden et al., 2006, Paster et al., 2006, Demmer et al., 2008c), shares several pathobiological features with RA(Rosenstein et al., 2004, Culshaw et al., 2011). Two recent small clinical trials have demonstrated that Periodontal therapy among RA patients can reduce RA disease activity(Al-Katma et al., 2007, Ortiz et al., 2009) providing evidence that Periodontal infections might exacerbate RA severity. Others have reported associations between periodontitis and RA in cross-sectional studies(de Pablo et al., 2008, Pischon et al., 2008, de Pablo et al., 2009). Such associations, however, may arise from shared environmental or genetic risk factors that result in similar pathobiology. Importantly, associations between periodontitis and RA have been observed following adjustment for smoking, which is the most important known shared environmental risk factor(de Pablo et al., 2008, de Pablo et al., 2009, Molitor, 2009). Thus, Periodontal disease pathobiology might contribute to the development of RA or vice versa. Longitudinal analyses can help to establish the temporal relationship between clinical Periodontal disease and RA. The only available longitudinal data that followed the development of RA subsequent to the assessment of Periodontal infection suggest increased incidence of RA in never smokers with moderate to severe periodontitis in the Atherosclerosis Risk in Communities (ARIC) cohort(Molitor, 2009). The First National Health and Nutrition Examination Survey (NHANES I) and its epidemiological follow – up study (NHEFS) provide a unique opportunity to examine the association between prevalent Periodontal disease and both prevalent and incident RA because: i) both medical and dental evaluations were conducted concurrently at baseline; and ii) the large nationally representative sample and long longitudinal follow-up period enabled the accumulation of adequate RA event rates. We tested the hypothesis that baseline evidence of historical exposure to Periodontal infections (assessed via clinical Periodontal Examination and tooth loss status) can predict both prevalent and incident RA in the nationally representative, population-based setting of NHANES I and NHEFS. Based on findings from the ARIC study(Molitor, 2009), we also hypothesized that the association with incident RA would be strongest in never smokers. We have included the cross-sectional aims in our current report to establish consistency with previous research.