Unraveling the Link between Periodontitis and Coronavirus Disease 2019: Exploring Pathogenic Pathways and Clinical Implications.
En-Chin LinYi-Chun ChiangHsuan-Yu LinShao-Yu TsengYu-Ting HsiehJer-An ShiehYu-Hao HuangHsiang-Tai TsaiSheng-Wei FengTzu-Yu PengI-Ta LeePublished in: Biomedicines (2023)
Periodontitis involves the inflammation of the periodontal tissue, leading to tissue loss, while coronavirus disease 2019 (COVID-19) is a highly transmissible respiratory disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is amplified by poor systemic health. Key facilitators of SARS-CoV-2's entry into host cells are angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2). This review reveals that periodontal pockets can serve as a hotspot for virus accumulation, rendering surrounding epithelia more susceptible to infection. Given that ACE2 is expressed in oral mucosa, it is reasonable to suggest that poor periodontal health could increase the risk of COVID-19 infection. However, recent studies have not provided sufficient evidence to imply a significant effect of COVID-19 on periodontal health, necessitating further and more long-term investigations. Nevertheless, there are hypotheses linking the mechanisms of the two diseases, such as the involvement of interleukin-17 (IL-17). Elevated IL-17 levels are observed in both COVID-19 and periodontitis, leading to increased osteoclast activity and bone resorption. Lastly, bidirectional relationships between periodontitis and systemic diseases like diabetes are acknowledged. Given that COVID-19 symptoms may worsen with these conditions, maintaining good oral health and managing systemic diseases are suggested as potential ways to protect against COVID-19.
Keyphrases
- coronavirus disease
- respiratory syndrome coronavirus
- sars cov
- angiotensin converting enzyme
- healthcare
- public health
- angiotensin ii
- mental health
- cardiovascular disease
- oral health
- health information
- type diabetes
- human health
- induced apoptosis
- cell cycle arrest
- pi k akt
- risk assessment
- soft tissue
- cell death
- glycemic control