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      Prospective Longitudinal Changes in the Periodontal Inflamed Surface Area Following Active Periodontal Treatment for Chronic Periodontitis

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          Abstract

          Periodontal disease is a chronic inflammatory disease of the periodontal tissue. The periodontal inflamed surface area (PISA) is a proposed index for quantifying the inflammatory burden resulting from periodontitis lesions. This study aimed to investigate longitudinal changes in the periodontal status as evaluated by the PISA following the active periodontal treatment. To elucidate the prognostic factors of PISA, mixed-effect modeling was performed for clinical parameters, tooth-type, and levels of periodontal pathogens as independent variables. One-hundred-twenty-five patients with chronic periodontitis who completed the active periodontal treatment were followed-up for 24 months, with evaluations conducted at 6-month intervals. Five-times repeated measures of mean PISA values were 130+/−173, 161+/−276, 184+/−320, 175+/−417, and 209+/−469 mm 2. Changes in clinical parameters and salivary and subgingival periodontal pathogens were analyzed by mixed-effect modeling. Plaque index, clinical attachment level, and salivary levels of Porphyromonas gingivalis were associated with changes in PISA at the patient- and tooth-level. Subgingival levels of P. gingivalis and Prevotella intermedia were associated with changes in PISA at the sample site. For most patients, changes in PISA were within 10% of baseline during the 24-month follow-up. However, an increase in the number of bleeding sites in a tooth with a deep periodontal pocket increased the PISA value exponentially.

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          Most cited references60

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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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            Polymicrobial synergy and dysbiosis in inflammatory disease.

            Uncontrolled inflammation of the periodontal area may arise when complex microbial communities transition from a commensal to a pathogenic entity. Communication among constituent species leads to polymicrobial synergy between metabolically compatible organisms that acquire functional specialization within the developing community. Keystone pathogens, even at low abundance, elevate community virulence, and the resulting dysbiotic community targets specific aspects of host immunity to further disable immune surveillance while promoting an overall inflammatory response. Inflammophilic organisms benefit from proteinaceous substrates derived from inflammatory tissue breakdown. Inflammation and dysbiosis reinforce each other, and the escalating environmental changes further select for a pathobiotic community. We have synthesized the polymicrobial synergy and dysbiotic components of the process into a new model for inflammatory diseases.
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              Periodontal inflamed surface area: quantifying inflammatory burden.

              Currently, a large variety of classifications is used for periodontitis as a risk factor for other diseases. None of these classifications quantifies the amount of inflamed periodontal tissue, while this information is needed to assess the inflammatory burden posed by periodontitis. To develop a classification of periodontitis that quantifies the amount of inflamed periodontal tissue, which can be easily and broadly applied. A literature search was conducted to look for a classification of periodontitis that quantified the amount of inflamed periodontal tissue. A classification that quantified the root surface area affected by attachment loss was found. This classification did not quantify the surface area of inflamed periodontal tissue, however. Therefore, an Excel spreadsheet was developed in which the periodontal inflamed surface area (PISA) is calculated using clinical Attachment Level (CAL), recessions and bleeding on probing (BOP). The PISA reflects the surface area of bleeding pocket epithelium in square millimetres. The surface area of bleeding pocket epithelium quantifies the amount of inflamed periodontal tissue. A freely downloadable spreadsheet is available to calculate the PISA. PISA quantifies the inflammatory burden posed by periodontitis and can be easily and broadly applied.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                10 March 2021
                March 2021
                : 10
                : 6
                : 1165
                Affiliations
                [1 ]Department of Translational Research, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan; nomura-y@ 123456tsurumi-u.ac.jp (Y.N.); hanada-n@ 123456tsurumi-u.ac.jp (N.H.)
                [2 ]Division of Periodontology, Department of Oral Interdisciplinary Medicine, Graduate School of Dentistry, Kanagawa Dental University, Yokosuka 238-8580, Japan; minabe@ 123456kdu.ac.jp
                [3 ]Department of Periodontology, Tokyo Dental College, Tokyo 101-0061, Japan; atsaito@ 123456tdc.ac.jp
                [4 ]Department of Periodontology and Endodontology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8588, Japan; ayoshi@ 123456nagasaki-u.ac.jp
                [5 ]Department of Oral Microbiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan; kakuta-erika@ 123456tsurumi-u.ac.jp
                [6 ]Division of Dental Anesthesiology, Department of Oral Surgery, Ohu University School of Dentistry, Koriyama 963-8611, Japan; f-suzuki@ 123456den.ohu-u.ac.jp
                [7 ]Section of Periodontology, Division of Oral Rehabilitation, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan; fusanori@ 123456dent.kyushu-u.ac.jp
                [8 ]Department of Periodontology, Nihon University School of Dentistry at Matsudo, Matsudo 271-8587, Japan; takai.hideki@ 123456nihon-u.ac.jp (H.T.); nakayama.youhei@ 123456nihon-u.ac.jp (Y.N.); ogata.yorimasa@ 123456nihon-u.ac.jp (Y.O.)
                [9 ]Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; h-kobayashi.peri@ 123456tmd.ac.jp
                [10 ]Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan; kazuperi@ 123456dent.kagoshima-u.ac.jp (K.N.); toshi-n@ 123456dent.kagoshima-u.ac.jp (T.N.)
                [11 ]Division of Periodontics, Department of Conservative Dentistry, Ohu University School of Dentistry, Koriyama 963-8611, Japan; ke-takahashi@ 123456den.ohu-u.ac.jp
                [12 ]Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8514, Japan; koichi@ 123456dent.niigata-u.ac.jp
                [13 ]Department of Periodontology, Osaka Dental University, Hirakata 573-1121, Japan; umeda-m@ 123456cc.osaka-dent.ac.jp
                [14 ]Department of Periodontology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan; fukuda-m@ 123456dpc.agu.ac.jp
                [15 ]Department of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan; sugano.naoyuki@ 123456nihon-u.ac.jp
                [16 ]Department of Periodontology, School of Dentistry, Matsumoto Dental University, Shiojiri 399-0781, Japan; nobuo.yoshinari@ 123456mdu.ac.jp
                [17 ]Department of Periodontology, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo 102-8159, Japan; sekino-s@ 123456tky.ndu.ac.jp (S.S.); numabe-y@ 123456tky.ndu.ac.jp (Y.N.)
                [18 ]Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8525, Japan; stakashi@ 123456okayama-u.ac.jp
                [19 ]Department of Periodontology, School of life Dentistry at Niigata, The Nippon Dental University, Niigata 951-8580, Japan; s-sato@ 123456ngt.ndu.ac.jp
                [20 ]Division of Periodontology and Endodontology, Department of Oral Health Science, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan; sugaya@ 123456den.hokudai.ac.jp
                [21 ]Department of Dentistry and Oral Surgery, School of Medicine, Keio University, Tokyo 160-8582, Japan; tane@ 123456z6.keio.jp
                Author notes
                [* ]Correspondence: morozumi@ 123456kdu.ac.jp ; Tel.: +81-46-822-8855
                Author information
                https://orcid.org/0000-0002-0814-0572
                https://orcid.org/0000-0002-7151-1292
                https://orcid.org/0000-0002-0065-2207
                https://orcid.org/0000-0002-5766-1286
                https://orcid.org/0000-0002-5156-9729
                https://orcid.org/0000-0002-9130-7256
                https://orcid.org/0000-0003-4248-1415
                https://orcid.org/0000-0003-2675-484X
                https://orcid.org/0000-0002-2767-844X
                Article
                jcm-10-01165
                10.3390/jcm10061165
                7998532
                81955048-197a-4d5e-ae39-6173aaa51c0b
                © 2021 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
                : 22 February 2021
                : 08 March 2021
                Categories
                Article

                periodontal inflamed surface area,periodontal pathogen,mixed effect modeling,follow-up study

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