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      Periodontal health

      1 , 2
      Journal of Clinical Periodontology
      Wiley

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          Porphyromonas gingivalis as a potential community activist for disease.

          An extensive analysis of dental plaque samples over the years has led to the identification of "red" complex oral bacteria that have a strong association with each other and with disease. Consequently, these bacteria have been labeled 'periopathogens'. Studies with one of these bacteria, Porphyromonas gingivalis, have revealed that it contains several different mechanisms which either impede or modulate periodontal protective mechanisms. In a mouse model of periodontitis, it has been shown that modulation of complement function by P. gingivalis facilitates a significant change in both the amount and composition of the normal oral microbiotia. This altered oral commensal microbiota is responsible for pathologic bone loss in the mouse. Thus, P. gingivalis creates a dysbiosis between the host and dental plaque, and this may represent one mechanism by which periodontitis can be initiated. We have therefore termed P. gingivalis a keystone pathogen.
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            Influence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance.

            Limited evidence exists on the significance of residual probing pocket depth (PPD) as a predictive parameter for periodontal disease progression and tooth loss. The aim of this study was to investigate the influence of residual PPD >or=5 mm and bleeding on probing (BOP) after active periodontal therapy (APT) on the progression of periodontitis and tooth loss. In this retrospective cohort, 172 patients were examined after APT and supportive periodontal therapy (SPT) for 3-27 years (mean 11.3 years). Analyses were conducted using information at site, tooth and patient levels. The association of risk factors with tooth loss and progression of periodontitis was investigated using multilevel logistic regression analysis. The number of residual PPD increased during SPT. Compared with PPD or=7 mm 37.9 and 64.2, respectively. At patient level, heavy smoking, initial diagnosis, duration of SPT and PPD>or=6 mm were risk factors for disease progression, while PPD>or=6 mm and BOP>or=30% represented a risk for tooth loss. Residual PPD>or=6 mm represent an incomplete periodontal treatment outcome and require further therapy.
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              Absence of bleeding on probing. An indicator of periodontal stability.

              Following active periodontal therapy, 41 patients were incorporated in a maintenance program for 2 1/2 years with recall intervals varying between 2-6 months. At the beginning of each maintenance visit, the periodontal tissues were evaluated using "bleeding on probing" (BOP). Reinstrumentation was only performed at sites which bled on probing. However, supragingival plaque and calculus was always removed. Pocket probing depths and probing attachment levels were recorded after active treatment and at the conclusion of the study. Progression of periodontal disease was defined by an observed loss of probing attachment of greater than or equal to 2 mm. The reliability of the BOP test as a predictor was evaluated by calculating sensitivity, specificity, accuracy, and positive and negative predictive values. While only a 29% sensitivity was calculated for frequent bleeding, the specificity was 88%. The fact that the positive predictive value for disease progression was only 6% and the negative predictive value was 98% renders continuous absence of BOP a reliable predictor for the maintenance of periodontal health.
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                Author and article information

                Journal
                Journal of Clinical Periodontology
                J Clin Periodontol
                Wiley
                03036979
                June 2018
                June 2018
                June 20 2018
                : 45
                : S9-S16
                Affiliations
                [1 ]Universities of Bern and Zurich; Switzerland
                [2 ]University of Adelaide; South Australia
                Article
                10.1111/jcpe.12936
                29926485
                3f07cd44-fd7b-4f8c-b430-99cea5b66874
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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