Smoking seriously affects oral health and causes a variety of oral diseases. Numerous clinical data show that smoking significantly increases the risk of periodontitis, and the duration and amount of smoking are positively correlated with the severity of periodontitis. In fact, smoking creates an environment conducive to the colonization of periodontopathogens, which affects the process of periodontitis. Since subgingival plaque which harbors periodontopathogens is the initiation factor of periodontitis, it is critical to study the impact of smoking on subgingival microbiota for understanding the relationship between smoking and periodontitis. Continuous advances have been made on the understanding of effects of smoking on subgingival plaque and the development of periodontitis. Smoking is observed to enhance the pathogenicity of periodontopathogens, especially the red complex microorganisms, via promoting their colonization and infection, and regulating the expression and function of multiple virulence factors. Furthermore, smoking has a negative impact on periodontal microecological homeostasis, which is reflected in the decrease of commensal bacteria and the increase of periodontopathogens, as well as the changes in the interaction between periodontopathogens and their commensal microbes in subgingival biofilm, thus influencing the pathogenicity of the subgingival plaque. In summary, the mechanism of smoking on subgingival plaque microorganisms represented by the red complex and its effect on the periodontal microecology still need to be further explored. The relevant research results are of great significance for guiding the periodontal clinical treatment of smoking population. This review summarizes the effects and relevant mechanisms of smoking on subgingival plaque and the development of periodontitis.

Macrophage M1 polarization mediated via the IL-6/STAT3 pathway contributes to apical periodontitis induced by Porphyromonas gingivalis Objective: To investigate the involvement of IL-6/STAT3 signaling pathway activation in macrophage polarization and bone destruction related to apical periodontitis (AP) stimulated by Porphyromonas gingivalis. Methodology: Macrophage polarization, IL-6/STAT3 expression, and the presence of P. gingivalis were detected in human AP tissues via RT-qPCR, western blotting, and immunohistochemistry staining. Murine bone marrow derived macrophages were isolated and cultured with P. gingivalis W83 in vitro, and levels of macrophage IL-6 expression, STAT3 phosphorylation, and macrophage polarization with or without the selective STAT3 phosphorylation inhibitor Stattic (5 μM) were detected via ELISA, western blotting, RT-qPCR, and flow cytometry, respectively. P. gingivalis-induced murine AP models were constructed, and bone destruction and macrophage polarization in the apical region were evaluated. Transwell co-culture systems were used to investigate the effects of macrophages infected with P. gingivalis on osteogenesis and osteoclastogenesis. Results: P. gingivalis was detected in human AP tissues that highly expressed IL-6/STAT3, and the M1 subtype of macrophages was more abundant in these tissues. P. gingivalis infection induced IL-6 expression, STAT3 phosphorylation, and M1 polarization of macrophages, while 5 μM of Stattic partially abolished these activation effects. Systemic STAT3 blockade via oral administration of Stattic at a dose of 25 mg kg-1 alleviated murine periapical bone resorption and apical infiltration of M1 macrophages induced by P. gingivalis infection in vivo. Furthermore, macrophages infected with P. gingivalis promoted bone destruction via secretion of IL-6, TNF-α, and RANKL, which hinder pre-osteoblast expression of Runx2 and accelerate preosteoclast expression of NFAT2. Conclusions: The activation of IL-6/STAT3 signaling pathway is involved in mediating macrophages M1 polarization in the P. gingivalis induced apical inflammatory context and may also be intimately involved in the bone loss caused by P. gingivalis infection, directing the M1 macrophage infiltration during the progression of AP.

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