Uncovering the Oral Dysbiotic Microbiota as Masters of Neutrophil Responses in the Pathobiology of Periodontitis

Abstract

Numerous bacterial species participate in the shift of the oral microbiome from beneficial to dysbiotic. The biggest challenge lying ahead of microbiologists, immunologists and dentists is the fact that the bacterial species act differently, although usually synergistically, on the host immune cells, including neutrophils, and on the surrounding tissues, making the investigation of single factors challenging. As biofilm is a complex community, the members interact with each other, which can be a key issue in future studies designed to develop effective treatments. To understand how a patient gets to the stage of the late-onset (previously termed chronic) periodontitis or develops other, in some cases life-threatening, diseases, it is crucial to identify the microbial composition of the biofilm and the mechanisms behind its pathogenicity. The members of the red complex (Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia) have long been associated as the cause of periodontitis and stayed in the focus of research. However, novel techniques, such as 16S clonal analysis, demonstrated that the oral microbiome diversity is greater than ever expected and it opened a new era in periodontal research. This review aims to summarize the current knowledge concerning bacterial participation beyond P. gingivalis and the red complex in periodontal inflammation mediated by neutrophils and to spread awareness about the associated diseases and pathological conditions.

Electroacupuncture regulates macrophage, neutrophil, and oral microbiota to alleviate alveolar bone loss and inflammation in experimental ligature‐induced periodontitis

“…Oral microbiome can influence the development of periodontitis by modulating the function of immune cells such as macrophages and neutrophils and their inflammatory factors (E. Xiao et al, 2017; Prucsi et al, 2021; Metcalfe et al, 2022). We first investigated the supragingival microbiome as in many previous LIP studies.…”

The impact of periodontitis on vascular endothelial dysfunction

“…Nevertheless, the underlying mechanisms keeping the stability of and triggering the change in the microbial community are still not well understood. The inhibitory phenotype of P. gingivalis, Tannerella forsythia (T. forsythia), and Treponema denticola (T. denticola), namely the red-complex periopathogens, against the host innate response might play a pivotal role during the transition from periodontal health to disease (Xu et al, 2020;Prucsi et al, 2021). Moreover, community-based attack of periodontal pathogens on the host also offers a new possibility for periodontal microbial shift.…”

Impact of Bifidobacterium animalis subsp. lactis HN019 probiotic in the prevention of periodontitis associated with immunosuppression

“…2,3 These last two bacteria are considered master species in the development of favorable conditions for the multiplication of late colonizers, due to their ability to decrease the effectiveness of neutrophils through the generation of superoxide and induction of apoptosis. 4,5 Moreover, these bacteria release collagenases and other proteases, interfering with the synthesis of inflammatory biomarkers such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP-1). 6,7 The most critical factor in the pathogenesis of periodontitis is the reinforced interaction between microbial dysbiosis and the highly destructive inflammatory process.…”

“…Disruption of microbiota‐host homeostasis leads to a state of dysbiosis that favors the growth and colonization of classic periodontal microorganisms such as Porphyromonas gingivalis , Treponema denticola , Tannerella forsythia, Fusobacterium nucleatum , and Prevotella intermedia 2,3 . These last two bacteria are considered master species in the development of favorable conditions for the multiplication of late colonizers, due to their ability to decrease the effectiveness of neutrophils through the generation of superoxide and induction of apoptosis 4,5 . Moreover, these bacteria release collagenases and other proteases, interfering with the synthesis of inflammatory biomarkers such as interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α, and monocyte chemotactic protein (MCP‐1) 6,7 …”