Abstract
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.
Highlights
Published: 14 January 2021In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)emerged in Wuhan, China
This review focuses on the potential role of pre-existing periodontal bacterial infection on the severity of COVID-19 in older people
Considering that aspiration pneumonia is often caused by P. gingivalis [110,120], and that oral bacteria have been identified in bronchoalveolar lavage samples from COVID-19 patients [121], there are at least three interconnected mechanisms that might facilitate
Summary
Young adults can be infected with SARS-CoV-2, the risk of developing severe COVID-19 increases with aging. Adults older than 65 years of age represent 80% of hospitalizations and have a higher risk of death compared with younger patients [2] This higher incidence of severe cases in older patients has generated the question whether basic cellular and molecular mechanisms of aging could be implicated in such susceptibility. Senescent cells gradually accumulate with chronological aging and contribute to the onset and development of chronic age-related pathologies including diabetes, cardiovascular disease, COPD, cerebrovascular inflammation, osteoporosis, and osteoarthritis [11,12,13,14,15,16]. We highlight that translocated Porphyromonas gingivalis, a prominent periodontal pathogen with highest prevalence in older adults, may facilitate SARS-CoV-2 replication in lung cells through different mechanisms. We consider how the inoculation of oral pathogens into the respiratory tract during invasive mechanical ventilation may aggravate SARS-CoV-2-mediated lung inflammation and immune response
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
