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      Lack of adjunctive effect of 0.1% sodium hypochlorite mouthwash combined to full‐mouth ultrasonic debridement on supragingival plaque, gingival inflammation, and subgingival microbiota: A randomized placebo‐controlled 6‐month trial

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          Abstract

          To test the adjunctive effect of 0.1% sodium hypochlorite (NaOCl) mouthwash combined to full‐mouth ultrasonic debridement (FMUD) on reducing supragingival plaque, gingival inflammation, and microbial pathogens. In this 6‐month double‐blinded randomized clinical trial, individuals with gingivitis were assigned to test ( n = 16) or placebo group ( n = 16) and received FMUD followed by rinsing with 0.1% NaOCl (test) or distilled water (placebo), respectively, twice a day for 1 month. Full‐mouth periodontal examination was performed at baseline, 1, 3, and 6 months posttherapy, and subgingival plaque samples were obtained at the same time points and analysed for their composition by checkerboard. Differences between groups over time were examined by Student t test, Mann–Whitney, generalized linear model, and Friedman and chi‐square tests. Both therapeutic protocols resulted in significant clinical improvement in periodontal parameters over time, except for probing depth and attachment level, which had a slight mean increase of 0.2 mm ( p < .01). No significant differences between groups were observed for any clinical parameter ( p > .05). Most species (>65%) decreased similarly in levels in both groups over time. Significant reductions in the microbial complexes were seen mainly at 1 and 3 months, but they returned to baseline levels in both groups, except for the red and yellow complexes, and other oral species, which were kept in low levels at 6 months ( p < .05). A 0.1% NaOCl mouthwash did not provide additional benefits to FMUD in reducing supragingival plaque, gingivitis, and/or microbial pathogens.

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          EXPERIMENTAL GINGIVITIS IN MAN.

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            Host response mechanisms in periodontal diseases

            Periodontal diseases usually refer to common inflammatory disorders known as gingivitis and periodontitis, which are caused by a pathogenic microbiota in the subgingival biofilm, including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Treponema denticola that trigger innate, inflammatory, and adaptive immune responses. These processes result in the destruction of the tissues surrounding and supporting the teeth, and eventually in tissue, bone and finally, tooth loss. The innate immune response constitutes a homeostatic system, which is the first line of defense, and is able to recognize invading microorganisms as non-self, triggering immune responses to eliminate them. In addition to the innate immunity, adaptive immunity cells and characteristic cytokines have been described as important players in the periodontal disease pathogenesis scenario, with a special attention to CD4+ T-cells (T-helper cells). Interestingly, the T cell-mediated adaptive immunity development is highly dependent on innate immunity-associated antigen presenting cells, which after antigen capture undergo into a maturation process and migrate towards the lymph nodes, where they produce distinct patterns of cytokines that will contribute to the subsequent polarization and activation of specific T CD4+ lymphocytes. Skeletal homeostasis depends on a dynamic balance between the activities of the bone-forming osteoblasts (OBLs) and bone-resorbing osteoclasts (OCLs). This balance is tightly controlled by various regulatory systems, such as the endocrine system, and is influenced by the immune system, an osteoimmunological regulation depending on lymphocyte- and macrophage-derived cytokines. All these cytokines and inflammatory mediators are capable of acting alone or in concert, to stimulate periodontal breakdown and collagen destruction via tissue-derived matrix metalloproteinases, a characterization of the progression of periodontitis as a stage that presents a significantly host immune and inflammatory response to the microbial challenge that determine of susceptibility to develop the destructive/progressive periodontitis under the influence of multiple behavioral, environmental and genetic factors.
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              Strengthening the prevention of periodontal disease: the WHO approach.

              The aim of this paper is to provide an overview of the burden of periodontal disease in adult populations worldwide, to emphasize the essential risk factors common to periodontal disease and chronic diseases, to outline important new strategies for effective prevention of periodontal disease, and to inform about the role of the World Health Organization (WHO) in developing a national capacity for the prevention of disease. Information about periodontal health status as measured by the Community Periodontal Index system is stored in the WHO Global Oral Health Data Bank. Updated information concerning WHO standard age groups was used to describe the prevalence rates of signs of periodontal disease, i.e., gingival bleeding, periodontal pocketing, and loss of attachment. Gingival bleeding is highly prevalent among adult populations in all regions of the world; advanced disease with deep periodontal pockets (> or =6 mm) affects approximately 10% to 15% of adults worldwide. The available evidence shows that important risk factors for periodontal disease relate to poor oral hygiene, tobacco use, excessive alcohol consumption, stress, and diabetes mellitus. Integrated preventive strategies based on the common risk factors approach are recommended for public health practice. The vast majority of countries need to establish a surveillance system for measuring progress in the control of periodontal disease and promotion of oral health. WHO has designed approaches for the integration of oral disease prevention within the prevention of non-communicable chronic diseases, and global strategies are currently being implemented in all regions of the world.
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                Author and article information

                Contributors
                apcolombo@micro.ufrj.br
                Journal
                Clin Exp Dent Res
                Clin Exp Dent Res
                10.1002/(ISSN)2057-4347
                CRE2
                Clinical and Experimental Dental Research
                John Wiley and Sons Inc. (Hoboken )
                2057-4347
                31 March 2017
                April 2017
                : 3
                : 2 ( doiID: 10.1002/cre2.v3.2 )
                : 51-61
                Affiliations
                [ 1 ] Department of Clinics, School of Dentistry Federal University of Rio de Janeiro Brazil
                [ 2 ] Department of Medical Microbiology, Institute of Microbiology Federal University of Rio de Janeiro Brazil
                Author notes
                [*] [* ] Correspondence

                Ana Paula V. Colombo, Instituto de Microbiologia Paulo de Góes, CCS/UFRJ, Bloco I, lab. I2‐03, Av. Carlos Chagas Filho, 373 Cidade Universitária, Rio de Janeiro, RJ CEP: 21941‐902, Brazil.

                Email: apcolombo@ 123456micro.ufrj.br

                Author information
                http://orcid.org/0000-0002-2061-1840
                Article
                CRE260 CRE2.20170009.R1
                10.1002/cre2.60
                5719817
                65440612-aed0-4494-b859-246b472659c6
                ©2017 The Authors. Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.

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

                History
                : 17 January 2017
                : 05 February 2017
                : 08 February 2017
                Page count
                Figures: 6, Tables: 1, Pages: 11, Words: 5167
                Funding
                Funded by: Conselho Nacional de Desenvolvimento Científico e Tecnológico
                Award ID: 302685/2013‐8
                Funded by: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
                Award ID: E‐26/201.162/2014
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                cre260
                April 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.5 mode:remove_FC converted:17.11.2017

                dental plaque,gingivitis,mouthwash,sodium hypochlorite
                dental plaque, gingivitis, mouthwash, sodium hypochlorite

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