Subgingival Microbiota and Cytokines Profile Changes in Patients with Periodontitis: A Pilot Study Comparing Healthy and Diseased Sites in the Same Oral Cavities.

Pauline Esparbès,Octave Nadile Bandiaky,Arnaud Legrand,Assem Soueidan,Marjorie Chéraud-Carpentier,Emmanuel Montassier,Hamida Martin

doi:10.3390/microorganisms9112364

Pauline Esparbès, Octave Nadile Bandiaky + Show 5 more

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https://doi.org/10.3390/microorganisms9112364

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Abstract

Periodontitis is a common condition characterized by an exacerbated pro-inflammatory response, which leads to tissue destruction and, ultimately, alveolar bone loss. In this pilot study, we assess the microbiota composition and cytokine profile changes in patients with stage III/IV, grade B/C periodontitis, specifically by comparing healthy and diseased sites in the same oral cavity. Overall, we found that microbiota architecture was significantly disrupted between diseased and healthy sites, and that the clustering was driven, in part, by the increased relative abundances of Synergistetes in diseased sites, as well as the increased abundances of Firmicutes in healthy sites. We also observed that diseased sites were enriched in Synergistetes, TM7, SR1, Spirochaetes, Bacteroidetes and Fusobacteria, and depleted in Firmicutes, Proteobacteria, Tenericutes and Actinobacteria compared to healthy sites. We found that Interleukin-1b, Interleukin-4, Interleukin-10, and Interleukin-17A were significantly overexpressed in diseased sites, whereas Interleukin-6 and TNF-alpha do not differ significantly between healthy and diseased sites. Here, we observed concomitant changes in the subgingival plaque microbiota and cytokines profile, suggesting that this combined alteration could contribute to the pathobiology of periodontitis.

Highlights

The stages of periodontitis were diagnosed on clinical charts and radiographic data according to the criteria of new classification
If we were unable to highlight correlations between the cytokines expression and dysbiosis indexes, our results showed that Interleukin-1b, Interleukin-4, Interleukin-10, and Interleukin-17A were significantly overexpressed in diseased sites, whereas Interleukin-6 and TNF-alpha did not differ significantly between healthy and diseased sites
Our study demonstrates that the altered oral microbiota in diseased sites affected the cytokines levels, demonstrating a significant positive correlation between proinflammatory TNF-α and taxa known to be associated with pathogenesis of periodontitis, such as Actinomyces, and Fusobacterium

Summary

Introduction

Periodontitis is a common condition for which the consequences gradually increase with age [1]. This chronic inflammation of tooth-supporting tissues is characterized by an exacerbated pro-inflammatory response, leading to tooth loss. Even though a detailed pathogenesis remains elusive, it is well accepted that bone destruction occurs in response to oral microbiota dysbiosis [2]. A new classification was proposed following the Chicago consensus conference in. 2017, co-presented by the American Academy of Periodontology (AAP) and the European. This new classification replaced the Armitage classification [3,4]. In the new classification scheme, the distinction between aggressive periodontitis

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