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      Ubiquitination in Periodontal Disease: A Review

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          Abstract

          Periodontal disease (periodontitis) is a chronic inflammatory condition initiated by microbial infection that leads to gingival tissue destruction and alveolar bone resorption. The periodontal tissue’s response to dental plaque is characterized by the accumulation of polymorphonuclear leukocytes, macrophages, and lymphocytes, all of which release inflammatory mediators and cytokines to orchestrate the immunopathogenesis of periodontal disease. Ubiquitination is achieved by a mechanism that involves a number of factors, including an ubiquitin-activating enzyme, ubiquitin-conjugating enzyme, and ubiquitin–protein ligase. Ubiquitination is a post-translational modification restricted to eukaryotes that are involved in essential host processes. The ubiquitin system has been implicated in the immune response, development, and programmed cell death. Increasing numbers of recent reports have provided evidence that many approaches are delivering promising reports for discovering the relationship between ubiquitination and periodontal disease. The scope of this review was to investigate recent progress in the discovery of ubiquitinated protein in diseased periodontium and to discuss the ubiquitination process in periodontal diseases.

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          Most cited references62

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          PERIODONTAL DISEASE IN PREGNANCY. II. CORRELATION BETWEEN ORAL HYGIENE AND PERIODONTAL CONDTION.

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            Ubiquitination in disease pathogenesis and treatment.

            Ubiquitination is crucial for a plethora of physiological processes, including cell survival and differentiation and innate and adaptive immunity. In recent years, considerable progress has been made in the understanding of the molecular action of ubiquitin in signaling pathways and how alterations in the ubiquitin system lead to the development of distinct human diseases. Here we describe the role of ubiquitination in the onset and progression of cancer, metabolic syndromes, neurodegenerative diseases, autoimmunity, inflammatory disorders, infection and muscle dystrophies. Moreover, we indicate how current knowledge could be exploited for the development of new clinical therapies.
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              Invasive potential of gut mucosa-derived Fusobacterium nucleatum positively correlates with IBD status of the host.

              Fusobacterium nucleatum is a heterogeneous oral pathogen that is also a common resident of the human gut mucosa. Given that some strains of F. nucleatum are known to be invasive and proinflammatory in the oral mucosa, we compared strains isolated from patients with inflammatory bowel disease (IBD) with strains isolated from healthy controls to determine 1) whether this species was more commonly associated with IBD patients; and 2) whether gut-derived F. nucleatum strains from IBD patients showed an increased capacity for invasion. Biopsy material was obtained from 56 adult patients undergoing colonoscopy for colon cancer screening purposes or assessment of irritable bowel syndrome status (34 patients), or to assess for presence of gastrointestinal disease (i.e., IBD or indeterminate colitis, 22 patients). We enumerated Fusobacterium spp. strains isolated from human gut biopsy material in a blinded fashion, and then compared the virulence potential of a subset of F. nucleatum strains using an invasion assay in a Caco-2 model system. Fusobacterium spp. were isolated from 63.6% of patients with gastrointestinal disease compared to 26.5% of healthy controls (P = 0.01). In total, 69% of all Fusobacterium spp. recovered from patients were identified as F. nucleatum. F. nucleatum strains originating from inflamed biopsy tissue from IBD patients were significantly more invasive in a Caco-2 cell invasion assay than strains that were isolated from healthy tissue from either IBD patients or control patients (P < 0.05 to 0.001). This study indicates that colonization of the intestinal mucosa by highly invasive strains of F. nucleatum may be a useful biomarker for gastrointestinal disease. Copyright © 2011 Crohn's & Colitis Foundation of America, Inc.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                10 July 2017
                July 2017
                : 18
                : 7
                : 1476
                Affiliations
                [1 ]Division of Clinical Mass Spectrometry, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; msatoh1995@ 123456yahoo.co.jp (M.S.); takiwaki@ 123456chiba-u.jp (M.T.); fnomura@ 123456faculty.chiba-u.jp (F.N.)
                [2 ]Division of Laboratory Medicine, Clinical Genetics and Proteomics, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
                Author notes
                [* ]Correspondence: sachio61@ 123456yahoo.co.jp ; Fax: +81-43-226-2169
                Article
                ijms-18-01476
                10.3390/ijms18071476
                5535967
                28698506
                42d8d49c-8db1-46f3-a4e8-b6a5c91079c9
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 27 April 2017
                : 05 July 2017
                Categories
                Review

                Molecular biology
                ubiquitination,proteasome,periodontal diseases
                Molecular biology
                ubiquitination, proteasome, periodontal diseases

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