Advances in the relationship between periodontopathogens and respiratory diseases (Review)

Abstract

Periodontitis is a common chronic inflammatory and destructive disease in the mouth and is considered to be associated with systemic diseases. Accumulating evidence has suggested that periodontitis is a risk factor for pulmonary diseases such as pneumonia, chronic obstructive pulmonary disease (COPD), asthma, coronavirus disease 2019 (COVID‑19) and lung cancer. The presence of common periodontal pathogens has been detected in samples from a variety of pulmonary diseases. Periodontal pathogens can be involved in lung diseases by promoting the adhesion and invasion of respiratory pathogens, regulating the apoptosis of respiratory epithelium and inducing overexpression of mucin and disrupting the balance of immune systemin respiratory epithelium cells. Additionally, measures to control plaque and maintain the health of periodontal tissue can decrease the incidence of respiratory adverse events. This evidence suggests a close association between periodontitis and pulmonary diseases. The present study aimed to review the clinical association between periodontitis and pneumonia, COPD, asthma, COVID‑19 and lung cancer, and propose a possible mechanism and potential role of periodontal pathogens in linking periodontal disease and lung disease. This could provide a direction for further research on the association between periodontitis and lung disease and provide novel ideas for the clinical diagnosis and treatment management of these two diseases.

Keywords: Fusobacterium nucleatum; Porphyromonas gingivalis; chronic obstructive pulmonary disease; lung disease; periodontal disease; pneumonia.

Figure 1.

Potential mechanisms of periodontal pathogens involved in respiratory diseases. Periodontitis is associated with a variety of respiratory diseases, such as pneumonia, asthma, COPD, COVID-19, lung cancer and cystic fibrosis. Periodontal bacteria, along with their virulence factors and pro-inflammatory cytokines, have the potential to enter the respiratory tract through aspiration or mechanical assisted ventilation, leading to pathogenic effects. Additionally, they can enter the bloodstream through ruptured periodontal pockets and reach the lungs, thereby playing a causative role in pulmonary disease: i) Periodontal bacteria and respiratory pathogens co-infect respiratory epithelial cells, leading to respiratory epithelial cell damage, apoptosis and potential fatality; ii) periodontal bacteria stimulate respiratory epithelial cells, resulting in increased expression of MUC5AC and excessive mucus production; iii) periodontal bacteria promote the expression of PAFR, ACE2 and TMPRSS2 in respiratory epithelial cells, facilitating the adhesion and binding of respiratory pathogens; and iv) periodontal bacteria can directly enter respiratory epithelial cells and release pro-inflammatory cytokines. Furthermore, systemic low inflammation caused by periodontal bacteria can modulate immune cells, disrupt the balance between Th17/Treg and induce Th17 cells to release pro-inflammatory cytokines. Created with BioRender.com. COPD, chronic obstructive pulmonary disease; COVID-19, coronavirus disease 2019; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; PAFR, platelet activating factor receptor; ACE2, angiotensin converting enzyme 2; TMPRSS2, transmembrane serine protease 2; IL, interleukin; Th, T helper cell; Treg, regulatory T cell; GM-CSF, granulocyte-macrophage colony-stimulating factor.