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      Association between periodontal pathogens and systemic disease

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          Abstract

          A growing body of literature suggests that there is a link between periodontitis and systemic diseases. These diseases include cardiovascular disease, gastrointestinal and colorectal cancer, diabetes and insulin resistance, and Alzheimer's disease, as well as respiratory tract infection and adverse pregnancy outcomes. The presence of periodontal pathogens and their metabolic by-products in the mouth may in fact modulate the immune response beyond the oral cavity, thus promoting the development of systemic conditions. A cause-and-effect relationship has not been established yet for most of the diseases, and the mediators of the association are still being identified. A better understanding of the systemic effects of oral microorganisms will contribute to the goal of using the oral cavity to diagnose and possibly treat non-oral systemic disease.

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          Most cited references76

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          Inflammation and Alzheimer's disease.

          Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
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            Diabetes mellitus and periodontal diseases.

            The purpose of this review is to provide the reader with practical knowledge concerning the relationship between diabetes mellitus and periodontal diseases. Over 200 articles have been published in the English literature over the past 50 years examining the relationship between these two chronic diseases. Data interpretation is often confounded by varying definitions of diabetes and periodontitis and different clinical criteria applied to prevalence, extent, and severity of periodontal diseases, levels of glycemic control, and complications associated with diabetes. This article provides a broad overview of the predominant findings from research published in English over the past 20 years, with reference to certain "classic" articles published prior to that time. This article describes current diagnostic and classification criteria for diabetes and answers the following questions: 1) Does diabetes affect the risk of periodontitis, and does the level of metabolic control of diabetes have an impact on this relationship? 2) Do periodontal diseases affect the pathophysiology of diabetes mellitus or the metabolic control of diabetes? 3) What are the mechanisms by which these two diseases interrelate? and 4) How do people with diabetes and periodontal disease respond to periodontal treatment? Diabetes increases the risk of periodontal diseases, and biologically plausible mechanisms have been demonstrated in abundance. Less clear is the impact of periodontal diseases on glycemic control of diabetes and the mechanisms through which this occurs. Inflammatory periodontal diseases may increase insulin resistance in a way similar to obesity, thereby aggravating glycemic control. Further research is needed to clarify this aspect of the relationship between periodontal diseases and diabetes.
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              The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis.

              Previous studies have shown conflicting results as to whether periodontitis (PD) is associated with increased risk of coronary heart disease (CHD). The aim of the current study was to evaluate whether such an association exists. A systematic review of the literature revealed 5 prospective cohort studies (follow-up >6 years), 5 case-control studies, and 5 cross-sectional studies that were eligible for meta-analysis. Individual studies were adjusted for confounding factors such as age, sex, diabetes mellitus, and smoking. The 3 study categories were analyzed separately. Heterogeneity of the studies was assessed by Cochran Q test. The studies were homogeneous; therefore, the Mantel-Haenszel fixed-effect model was used to compute common relative risk and odds ratio (OR). Meta-analysis of the 5 prospective cohort studies (86092 patients) indicated that individuals with PD had a 1.14 times higher risk of developing CHD than the controls (relative risk 1.14, 95% CI 1.074-1.213, P < .001). The case-control studies (1423 patients) showed an even greater risk of developing CHD (OR 2.22, 95% CI 1.59-3.117, P < .001). The prevalence of CHD in the cross-sectional studies (17724 patients) was significantly greater among individuals with PD than in those without PD (OR 1.59, 95% CI 1.329-1.907, P < .001). When the relationship between number of teeth and incidence of CHD was analyzed, cohort studies showed 1.24 times increased risk (95% CI 1.14-1.36, P < .0001) of development of CHD in patients with <10 teeth. This meta-analysis indicates that both the prevalence and incidence of CHD are significantly increased in PD. Therefore, PD may be a risk factor for CHD. Prospective studies are required to prove this assumption and evaluate risk reduction with the treatment of PD.
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                Author and article information

                Contributors
                Journal
                Biomed J
                Biomed J
                Biomedical Journal
                Chang Gung University
                2319-4170
                2320-2890
                02 March 2019
                February 2019
                02 March 2019
                : 42
                : 1
                : 27-35
                Affiliations
                [a ]Department of Biomedical Sciences, University of the Pacific, Arthur Dugoni School of Dentistry, San Francisco, CA, USA
                [b ]Immunobiology Program, Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
                Author notes
                [] Corresponding author. Department of Biomedical Sciences, University of the Pacific, Arthur Dugoni School of Dentistry, 155 Fifth Street, San Francisco, CA 94103, USA. dojcius@ 123456pacific.edu
                [1]

                Equal first authors.

                Article
                S2319-4170(18)30263-4
                10.1016/j.bj.2018.12.001
                6468093
                30987702
                50205a38-8bde-416e-8904-7644f0321095
                © 2018 Chang Gung University. Publishing services by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 10 June 2018
                : 4 December 2018
                Categories
                Review Article

                oral pathogens,systemic disease,periodontal disease,chronic disease,inflammation,dentistry

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