Periodontal bacteria dissemination into the lower respiratory tract may create favorable conditions for severe COVID-19 lung infection. Once lung tissues are colonized, cells that survive persistent bacterial infection can undergo permanent damage and accelerated cellular senescence. Consequently, several morphological and functional features of senescent lung cells facilitate SARS-CoV-2 replication. The higher risk for severe SARS-CoV-2 infection, the virus that causes COVID-19, and death in older patients has generated the question whether basic aging mechanisms could be implicated in such susceptibility. Mounting evidence indicates that cellular senescence, a manifestation of aging at the cellular level, contributes to the development of age-related lung pathologies and facilitates respiratory infections. Apparently, a relationship between life-threatening COVID-19 lung infection and pre-existing periodontal disease seems improbable. However, periodontal pathogens can be inoculated during endotracheal intubation and/or aspirated into the lower respiratory tract. This review focuses on how the dissemination of periodontal bacteria into the lungs could aggravate age-related senescent cell accumulation and facilitate more efficient SARS-CoV-2 cell attachment and replication. We also consider how periodontal bacteria-induced premature senescence could influence the course of COVID-19 lung infection. Finally, we highlight the role of saliva as a reservoir for both pathogenic bacteria and SARS-CoV-2. Therefore, the identification of active severe periodontitis can be an opportune and valid clinical parameter for risk stratification of old patients with COVID-19.
Keywords: COVID-19; LPS; Porphyromonas gingivalis; SARS-CoV-2; cellular senescence; lung; oral bacteria; periodontal disease; periodontitis; pneumonia.