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      Cellular expression of DNA damage/repair and reactive oxygen/nitrogen species in human periodontitis and peri‐implantitis lesions

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          Abstract

          Aim of the study

          To evaluate differences in the cellular expression of DNA damage/repair and reactive oxygen/nitrogen species between human periodontitis and peri‐implantitis lesions.

          Material and methods

          40 patients presenting with generalized severe periodontitis and 40 patients with severe peri‐implantitis were included. Soft tissue biopsies were collected from diseased sites in conjunction with surgical therapy and prepared for histological analysis. Four regions of interest were identified: the pocket epithelium (PE), the infiltrated connective tissue (ICT), which was divided into one inner area facing the PE (ICT‐1) and one outer area (ICT‐2). A non‐infiltrated connective tissue area (NCT) lateral of the ICT was also selected.

          Results

          It was demonstrated that the ICT of peri‐implantitis specimens was considerably larger and contained significantly larger area proportions and densities of CD68‐, MPO‐ and iNOS‐positive cells than that of periodontitis samples. Cellular densities were overall higher in the inner ICT zone lateral of the PE (ICT‐1) than in the outer ICT compartment (ICT‐2). While the NCT area lateral of the ICT comprised significantly larger proportions and densities of y‐H2AX‐, iNOS‐, NOX2‐, MPO‐ and PAD4/MPO‐positive cells in peri‐implantitis than in periodontitis sites, a reverse difference was noted for the area proportion and density of 8‐OHdG‐positive cells in the PE.

          Conclusions

          It is suggested that peri‐implantitis lesions are associated with an enhanced and upregulated host response and contain larger numbers of neutrophils, macrophages and iNOS‐positive cells than periodontitis lesions.

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          Most cited references39

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          The DNA-damage response in human biology and disease.

          The prime objective for every life form is to deliver its genetic material, intact and unchanged, to the next generation. This must be achieved despite constant assaults by endogenous and environmental agents on the DNA. To counter this threat, life has evolved several systems to detect DNA damage, signal its presence and mediate its repair. Such responses, which have an impact on a wide range of cellular events, are biologically significant because they prevent diverse human diseases. Our improving understanding of DNA-damage responses is providing new avenues for disease management.
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            The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

            For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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              Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions: Classification and case definitions for periodontitis

              A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.
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                Author and article information

                Contributors
                tord.berglundh@odontologi.gu.se
                Journal
                J Clin Periodontol
                J Clin Periodontol
                10.1111/(ISSN)1600-051X
                JCPE
                Journal of Clinical Periodontology
                John Wiley and Sons Inc. (Hoboken )
                0303-6979
                1600-051X
                09 November 2020
                December 2020
                : 47
                : 12 ( doiID: 10.1111/jcpe.v47.12 )
                : 1466-1475
                Affiliations
                [ 1 ] Department of Periodontology Institute of Odontology Sahlgrenska Academy University of Gothenburg Gothenburg Sweden
                Author notes
                [*] [* ] Correspondence

                Tord Berglundh, Department of Periodontology, Institute of Odontology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

                Email: tord.berglundh@ 123456odontologi.gu.se

                Author information
                https://orcid.org/0000-0001-5864-6398
                Article
                JCPE13370
                10.1111/jcpe.13370
                7756411
                32996143
                8a687623-4344-45b9-ad08-88ad22a0f4bd
                © 2020 The Authors. Journal of Clinical Periodontology published by John Wiley & Sons Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 30 June 2020
                : 14 September 2020
                : 15 September 2020
                Page count
                Figures: 2, Tables: 4, Pages: 10, Words: 7007
                Funding
                Funded by: Vetenskapsrådet , open-funder-registry 10.13039/501100004359;
                Award ID: 2016‐01571
                Funded by: TUA Research Funding University of Gothenburg /Region Västra Götaland, Sweden
                Categories
                Original Article Clinical Periodontology
                Periodontal Diseases
                Custom metadata
                2.0
                December 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.6 mode:remove_FC converted:23.12.2020

                Dentistry
                biopsy,cell density,histology,immunohistochemistry,inflammation,peri‐implant disease,periodontal disease

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