Athina Christina Georgiou1, Wim Crielaard2, Iakovos Armenis3, Ralph de Vries4, Suzette V van der Waal5. 1. Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Vrije Universiteit, Amsterdam, the Netherlands. Electronic address: a.c.georgiou@acta.nl. 2. Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Vrije Universiteit, Amsterdam, the Netherlands. 3. Department of Cardiology, Onassis Cardiac Surgery Centre, Athens, Greece; Department of Internal Medicine, "Laiko" Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece. 4. Medical Library, Vrije Universiteit, Amsterdam, the Netherlands. 5. Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Vrije Universiteit, Amsterdam, the Netherlands; Department of Endodontics, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Vrije Universiteit, Amsterdam, the Netherlands.
Abstract
INTRODUCTION: Apical periodontitis (AP), except for the local known consequences, may also be a systemic burden. Circulating inflammatory mediators that are released to sustain the AP lesion can in theory harm other bodily tissues. The aim of this systematic review was to summarize the existing evidence on the influence of AP on the peripheral blood levels of inflammatory mediators and markers of systemic stress. METHODS: A search of MEDLINE-PubMed, Embase, and Cochrane was conducted up to and including February 2019 to identify studies in 5 different languages. The Newcastle-Ottawa Scale was used for quality assessment of the included studies. RESULTS: Twelve of the 20 included studies were case-control studies, and 8 were intervention studies. The data of all the included studies were analyzed descriptively, whereas the data of 11 studies were available for meta-analyses. The study designs were heterogeneous. Nevertheless, the meta-analyses revealed statistically significant differences in C-reactive protein, interleukin 6, and asymmetric dimethylarginine levels between AP subjects and controls in peripheral blood. In addition, the concentration of C3 complement fragment in peripheral blood was significantly lower after the treatment and resolution of AP than before. CONCLUSIONS: The existing literature indicates that AP adds on to systemic inflammation by elevating C-reactive protein, interleukin 6, asymmetric dimethylarginine, and C3 levels. In order to overcome the issue of large variation between study designs, future studies should have clear inclusion criteria, preferably larger cohorts, adequate follow-up of all subjects, and a thorough presentation of the data to enable further exploration of the possible burden of AP on general human health. Nevertheless, there is now stronger evidence that AP contributes to low-grade systemic inflammation.
INTRODUCTION:Apical periodontitis (AP), except for the local known consequences, may also be a systemic burden. Circulating inflammatory mediators that are released to sustain the AP lesion can in theory harm other bodily tissues. The aim of this systematic review was to summarize the existing evidence on the influence of AP on the peripheral blood levels of inflammatory mediators and markers of systemic stress. METHODS: A search of MEDLINE-PubMed, Embase, and Cochrane was conducted up to and including February 2019 to identify studies in 5 different languages. The Newcastle-Ottawa Scale was used for quality assessment of the included studies. RESULTS: Twelve of the 20 included studies were case-control studies, and 8 were intervention studies. The data of all the included studies were analyzed descriptively, whereas the data of 11 studies were available for meta-analyses. The study designs were heterogeneous. Nevertheless, the meta-analyses revealed statistically significant differences in C-reactive protein, interleukin 6, and asymmetric dimethylarginine levels between AP subjects and controls in peripheral blood. In addition, the concentration of C3 complement fragment in peripheral blood was significantly lower after the treatment and resolution of AP than before. CONCLUSIONS: The existing literature indicates that AP adds on to systemic inflammation by elevating C-reactive protein, interleukin 6, asymmetric dimethylarginine, and C3 levels. In order to overcome the issue of large variation between study designs, future studies should have clear inclusion criteria, preferably larger cohorts, adequate follow-up of all subjects, and a thorough presentation of the data to enable further exploration of the possible burden of AP on general human health. Nevertheless, there is now stronger evidence that AP contributes to low-grade systemic inflammation.
Authors: Stella M F Lima; Mirna S Freire; Ana Paula C Cantuária; Danilo C M Martins; Ingrid A Amorim; Elaine M G L Dantas; Jade O Farias; Márcio B Castro; Jackson S Silva; Fernando A Barriviera; Maurício Barriviera; Jeeser A Almeida; Isadora A Uehara; Marcelo J B Silva; Ana Paula L Oliveira; Osmar N Silva; Robert E W Hancock; Octávio L Franco; Taia M B Rezende Journal: Clin Oral Investig Date: 2020-11-16 Impact factor: 3.573
Authors: Tom S Decates; Elmer C Kruijt Spanjer; Renu Saini; Peter J Velthuis; Frank M Niessen Journal: Dermatol Ther Date: 2020-06-30 Impact factor: 2.851