Association of Oral Microbiome with Host Defense Inflammatory Responses in Periodontitis: A Systematic Review

Abstract

Background: Periodontitis is a chronic inflammatory process that is caused by complex interactions between the oral microbiome and host immune responses, which cause the destruction of periodontal tissues and ultimately tooth loss. Presently, there is growing evidence that microbial dysbiosis is an important part of the initiation of inflammatory pathways and host defense mechanisms not only by individual bacterial pathogens. The association, however, between the changes of oral microflora and inflammatory reaction is still complex and needs to be further examined.

Objective: To critically appraise the relationship between oral microbiome changes and inflammatory response in host defence mechanisms in periodontitis.

Methods: The PRISMA guidelines were followed for a systematic review. PubMed, Embase, Scopus, Web of Science, and Google Scholar were used for searching electronic databases that included studies assessing the association between the oral microbiome properties and inflammatory reaction in periodontitis. Studies conducted in humans using observational methods, such as cross-sectional, cohort and case-control studies, were included. The study characteristics, analysis of the microbiome, changes in the microbiome, inflammatory biomarkers, and immune mechanisms were extracted. Newcastle-Ottawa scale was used to evaluate the methodological quality of studies included in the analysis. A narrative synthesis was done because of the heterogeneity of the studies.

Results: Fifteen studies were included in the systematic review. The results showed that there were remarkable changes in oral microbial community, an increase in periodontal pathogens, and a disturbance in oral microbial homeostasis in patients with periodontitis. Periodontal inflammation and tissue destruction were often associationed with the presence of pathogens such as Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. Microbial dysbiosis was correlated with the activation of host immune pathways, including activation of TLR and NF-κB pathways, leading to the generation of inflammatory mediators, such as IL-1β, IL-6, IL-8, TNF-α, and matrix metalloproteinases. Immune cell activation, osteoclast-mediated bone resorption and periodontal disease were associationed to microbial diversity and functional alterations of microbial communities.

Conclusion: This evidence suggests that periodontitis is a microbial–immune interaction disorder where dysbiosis of the oral microbiome produces an exaggerated inflammatory response of the host that leads to periodontal destruction. Knowing more about the role of the microbiome in inflammatory processes could help to develop more effective biomarkers and new therapeutic approaches focusing on the microbiome. Longitudinal studies that combine microbial and immune profiling in the future are needed to elucidate causal pathways and individualize the management of periodontal disease.