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      Exercise habituation is effective for improvement of periodontal disease status: a prospective intervention study

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          Background and purpose

          Periodontal disease is closely related to lifestyle-related diseases and obesity. It is widely known that moderate exercise habits lead to improvement in lifestyle-related diseases and obesity. However, little research has been undertaken into how exercise habits affect periodontal disease. The purpose of this study was to examine the effect of exercise habits on periodontal diseases and metabolic pathology.


          We conducted a prospective intervention research for 12 weeks. The subjects were 71 obese men who participated in an exercise and/or dietary intervention program. Fifty subjects were assigned to exercise interventions (exercise intervention group) and 21 subjects were assigned to dietary interventions (dietary intervention group). This research was conducted before and after each intervention program.


          In the exercise intervention group, the number of teeth with a probing pocket depth (PPD) ≥4 mm significantly decreased from 14.4% to 5.6% ( P<0.001), and the number of teeth with bleeding on probing (BOP) significantly decreased from 39.8% to 14.4% ( P<0.001). The copy counts of Tannerella forsythia and Treponema denticola decreased significantly ( P=0.001). A positive correlation was found between the change in the copy count of T. denticola and the number of teeth with PPD ≥4 mm ( P=0.003) and the number of teeth with BOP ( P=0.010). A positive correlation was also found between the change in the copy count of T. denticola and body weight ( P=0.008), low-density lipoprotein cholesterol ( P=0.049), and fasting insulin ( P=0.041). However, in the dietary intervention group the copy count of T. denticola decreased significantly ( P=0.007) and there was no correlation between the number of periodontal disease-causing bacteria and PPD and BOP.


          Our results are the first to show that exercise might contribute to improvements in periodontal disease.

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          Most cited references 41

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          Immune function in sport and exercise.

          Regular moderate exercise is associated with a reduced incidence of infection compared with a completely sedentary state. However, prolonged bouts of strenuous exercise cause a temporary depression of various aspects of immune function (e.g., neutrophil respiratory burst, lymphocyte proliferation, monocyte antigen presentation) that usually lasts approximately 3-24 h after exercise, depending on the intensity and duration of the exercise bout. Postexercise immune function dysfunction is most pronounced when the exercise is continuous, prolonged (>1.5 h), of moderate to high intensity (55-75% maximum O(2) uptake), and performed without food intake. Periods of intensified training (overreaching) lasting 1 wk or more may result in longer lasting immune dysfunction. Although elite athletes are not clinically immune deficient, it is possible that the combined effects of small changes in several immune parameters may compromise resistance to common minor illnesses, such as upper respiratory tract infection. However, this may be a small price to pay as the anti-inflammatory effects of exercise mediated through cytokines and/or downregulation of toll-like receptor expression are likely mediators of many of the long-term health benefits of regular exercise.
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            Periodontal disease and diabetes mellitus: a two-way relationship.

            Severe periodontal disease often coexists with severe diabetes mellitus. Diabetes is a risk factor for severe periodontal disease. A model is presented whereby severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. We propose that an infection-mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from lipopolysaccharide (LPS) and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response operative in diabetes mellitus. In this model, the combination of these 2 pathways, infection and AGE-mediated cytokine upregulation, helps explain the increase in tissue destruction seen in diabetic periodontitis, and how periodontal infection may complicate the severity of diabetes and the degree of metabolic control, resulting in a 2-way relationship between diabetes mellitus and periodontal disease/infection. This proposed dual pathway of tissue destruction suggests that control of chronic periodontal infection is essential for achieving long-term control of diabetes mellitus. Evidence is presented to support the hypothesis that elimination of periodontal infection by using systemic antibiotics improves metabolic control of diabetes, defined by reduction in glycated hemoglobin or reduction in insulin requirements.
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              Obesity increases sensitivity to endotoxin liver injury: implications for the pathogenesis of steatohepatitis.

              Genetically obese fatty/fatty rats and obese/obese mice exhibit increased sensitivity to endotoxin hepatotoxicity, quickly developing steatohepatitis after exposure to low doses of lipopolysaccharide (LPS). Among obese animals, females are more sensitive to endotoxin liver injury than males. LPS induction of tumor necrosis factor alpha (TNF alpha), the proven affecter of endotoxin liver injury, is no greater in the livers, white adipose tissues, or sera of obese animals than in those of lean controls. Indeed, the lowest serum concentrations of TNF occur in female obese rodents, which exhibit the most endotoxin-induced liver injury. Several cytokines that modulate the biological activity of TNF are regulated abnormally in the livers of obese animals. After exposure to LPS, mRNA of interferon gamma, which sensitizes hepatocytes to TNF toxicity, is overexpressed, and mRNA levels of interleukin 10, a TNF inhibitor, are decreased. The phagocytic activity of liver macrophages and the hepatic expression of a gene encoding a macrophage-specific receptor are also decreased in obesity. This new animal model of obesity-associated liver disease demonstrates that hepatic macrophage dysfunction occurs in obesity and suggests that this might promote steatohepatitis by sensitizing hepatocytes to endotoxin.

                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                20 March 2018
                : 14
                : 565-574
                [1 ]Oral and Maxillofacial Surgery, Clinical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan
                [2 ]Department of Dental Oral Surgery, Kitaibaraki City Hospital, Kitaibaraki, Ibaraki, Japan
                [3 ]Department of Oral and Maxillofacial Surgery, University of Tsukuba Hospital, Tsukuba, Ibaraki, Japan
                [4 ]Department of Medical Sciences, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
                [5 ]The Center of Sports Medicine and Health Sciences, Tsukuba University Hospital, Tsukuba, Ibaraki, Japan
                [6 ]Research Center for Overwork-Related Disorders, National Institute of Occupational Safety and Health, Kawasaki, Kanagawa, Japan
                [7 ]Department of Sports Medicine, Faculty of Human Sciences, Shimane University, Matsue, Shimane, Japan
                [8 ]Department of Oral and Maxillofacial Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
                [9 ]Department of Sports Medicine, Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan
                Author notes
                Correspondence: Fumihiko Uchida, Department of Oral and Maxillofacial Surgery, University of Tsukuba Hospital, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan, Tel +81 29 853 3052, Fax +81 29 853 3052, Email uchiyamada1031@ 123456yahoo.co.jp
                © 2018 Omori et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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