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      Periodontal Infection, Systemic Inflammation, and Insulin Resistance : Results from the continuous National Health and Nutrition Examination Survey (NHANES) 1999–2004

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          Abstract

          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 < 0.05). Among participants with WBC ≤6.4 × 10 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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          Most cited references26

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          Global prevalence of diabetes: estimates for the year 2000 and projections for 2030.

          The goal of this study was to estimate the prevalence of diabetes and the number of people of all ages with diabetes for years 2000 and 2030. Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and applied to United Nations' population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries. The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people >65 years of age. These findings indicate that the "diabetes epidemic" will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.
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            Case definitions for use in population-based surveillance of periodontitis.

            Many definitions of periodontitis have been used in the literature for population-based studies, but there is no accepted standard. In early epidemiologic studies, the two major periodontal diseases, gingivitis and periodontitis, were combined and considered to be a continuum. National United States surveys were conducted in 1960 to 1962, 1971 to 1974, 1981, 1985 to 1986, 1988 to 1994, and 1999 to 2000. The case definitions and protocols used in the six national surveys reflect a continuing evolution and improvement over time. Generally, the clinical diagnosis of periodontitis is based on measures of probing depth (PD), clinical attachment level (CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bleeding on probing, or a combination of these measures. Several other patient characteristics are considered, and several factors, such as age, can affect measurements of PD and CAL. Accuracy and reproducibility of measurements of PD and CAL are important because case definitions for periodontitis are based largely on either or both measurements, and relatively small changes in these values can result in large changes in disease prevalence. The classification currently accepted by the American Academy of Periodontology (AAP) was devised by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. However, in 2003 the Centers for Disease Control and Prevention and the AAP appointed a working group to develop further standardized clinical case definitions for population-based studies of periodontitis. This classification defines severe periodontitis and moderate periodontitis in terms of PD and CAL to enhance case definitions and further demonstrates the importance of thresholds of PD and CAL and the number of affected sites when determining prevalence.
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              IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance.

              Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.
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                Author and article information

                Journal
                Diabetes Care
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                November 2012
                13 October 2012
                : 35
                : 11
                : 2235-2242
                Affiliations
                [1] 1Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York
                [2] 2Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, New York
                [3] 3Departments of Pediatrics and Medicine, Division of Molecular Genetics, Columbia University, New York, New York
                [4] 4College of Physicians and Surgeons, Columbia University, New York, New York
                [5] 5Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
                [6] 6Department of Nutrition, University of Oslo, Oslo, Norway
                [7] 7INSERM, U738, Paris, France
                Author notes
                Corresponding author: Ryan T. Demmer, rtd2106@ 123456columbia.edu .
                Article
                0072
                10.2337/dc12-0072
                3476901
                22837370
                9b1aad18-8d10-4c4c-8ae6-cac6401892f7
                © 2012 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 11 January 2012
                : 12 May 2012
                Categories
                Original Research
                Epidemiology/Health Services Research

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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