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Associations between the number of natural teeth and renal dysfunction

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      The purpose of the present study was to investigate the association between the number of natural teeth and measures of kidney dysfunction, such as urinary albumin/creatinine ratio (ACR) and estimated glomerular filtration (eGFR) rate, using nationally representative data.

      The data used were from the Korea National Health and Nutrition Examination Survey with cross-sectional design, which was conducted between 2011 and 2012; the sample analyzed in this study consisted of a total of 10,388 respondents, each of whom was 19 years or older and had no missing outcome variables. The association between the number of natural teeth and kidney function was assessed by multiple logistic regression and model was adjusted for age, sex, waist conference, smoking, drinking, exercise, education, income, frequency of tooth brushing per day, diabetes, metabolic syndrome, urinary ACR, and eGFR.

      The mean age, body mass index, and waist circumference were significantly higher among those with lower kidney function (urinary ACR ≥30 mg/g and eGFR <60 mL/min/1.73m 2). Urinary ACR and eGFR were associated with loss of natural teeth. As urinary ACR increased, the number of natural teeth decreased accordingly. Conversely, the number of natural teeth increased with an increase in eGFR.

      This study showed that the number of natural teeth is inversely associated with the presence of kidney disease. Severity of tooth loss may be considered an independent risk indicator for kidney disease among Koreans. More epidemiological studies are warranted to investigate the role of tooth loss in kidney disease, to confirm this relationship and to test possible underlying mechanisms.

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       ,  John W. Kusek,  Tom Greene (2006)
      Glomerular filtration rate (GFR) estimates facilitate detection of chronic kidney disease but require calibration of the serum creatinine assay to the laboratory that developed the equation. The 4-variable equation from the Modification of Diet in Renal Disease (MDRD) Study has been reexpressed for use with a standardized assay. To describe the performance of the revised 4-variable MDRD Study equation and compare it with the performance of the 6-variable MDRD Study and Cockcroft-Gault equations. Comparison of estimated and measured GFR. 15 clinical centers participating in a randomized, controlled trial. 1628 patients with chronic kidney disease participating in the MDRD Study. Serum creatinine levels were calibrated to an assay traceable to isotope-dilution mass spectrometry. Glomerular filtration rate was measured as urinary clearance of 125I-iothalamate. Mean measured GFR was 39.8 mL/min per 1.73 m2 (SD, 21.2). Accuracy and precision of the revised 4-variable equation were similar to those of the original 6-variable equation and better than in the Cockcroft-Gault equation, even when the latter was corrected for bias, with 90%, 91%, 60%, and 83% of estimates within 30% of measured GFR, respectively. Differences between measured and estimated GFR were greater for all equations when the estimated GFR was 60 mL/min per 1.73 m2 or greater. The MDRD Study included few patients with a GFR greater than 90 mL/min per 1.73 m2. Equations were not compared in a separate study sample. The 4-variable MDRD Study equation provides reasonably accurate GFR estimates in patients with chronic kidney disease and a measured GFR of less than 90 mL/min per 1.73 m2. By using the reexpressed MDRD Study equation with the standardized serum creatinine assay, clinical laboratories can report more accurate GFR estimates.
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        Homeostatic model assessment (HOMA) is a method for assessing beta-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin or C-peptide concentrations. It has been reported in >500 publications, 20 times more frequently for the estimation of IR than beta-cell function. This article summarizes the physiological basis of HOMA, a structural model of steady-state insulin and glucose domains, constructed from physiological dose responses of glucose uptake and insulin production. Hepatic and peripheral glucose efflux and uptake were modeled to be dependent on plasma glucose and insulin concentrations. Decreases in beta-cell function were modeled by changing the beta-cell response to plasma glucose concentrations. The original HOMA model was described in 1985 with a formula for approximate estimation. The computer model is available but has not been as widely used as the approximation formulae. HOMA has been validated against a variety of physiological methods. We review the use and reporting of HOMA in the literature and give guidance on its appropriate use (e.g., cohort and epidemiological studies) and inappropriate use (e.g., measuring beta-cell function in isolation). The HOMA model compares favorably with other models and has the advantage of requiring only a single plasma sample assayed for insulin and glucose. In conclusion, the HOMA model has become a widely used clinical and epidemiological tool and, when used appropriately, it can yield valuable data. However, as with all models, the primary input data need to be robust, and the data need to be interpreted carefully.
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          Systemic diseases caused by oral infection.

          Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host's susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.

            Author and article information

            [a ]Department of Internal Medicine, Seonam University Myongji Hospital, Goyang, Gyeonggi-do
            [b ]Department of Biostatistics
            [c ]Department of Periodontics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
            Author notes
            []Correspondence: Jun-Beom Park, Department of Periodontics, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222, Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea (e-mail: jbassoonis@ ).
            Medicine (Baltimore)
            Medicine (Baltimore)
            Wolters Kluwer Health
            August 2016
            26 August 2016
            : 95
            : 34
            27559974 5400341 10.1097/MD.0000000000004681 04681
            Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.

            This is an open access article distributed under the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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            Observational Study
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