J Oral Med Oral Surg
Volume 27, Number 1, 2021
|Number of page(s)||2|
|Published online||11 December 2020|
Letter to the Editor
COVID-19 and risk of inflammatory periodontal disease initiation/progression: a hypothesis for future
Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Kurdistan University of Medical Sciences, Sanandaj, Iran
* Correspondence: firstname.lastname@example.org
Accepted: 5 October 2020
After reading the interest correspondence of Chaux-Bodard et al. “Oral manifestation of Covid-19 as an inaugural symptom?”  I thought about possibility of oral tissue manifestations/injuries resulted by this disease.
Coronavirus Disease-2019 (COVID-19) is caused by a novel coronavirus namely severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which utilizes cell surface angiotensin-converting enzyme 2 (ACE2) as receptor to cell entry . It is suggested that the oral cavity could be considered as a potentially high risk for SARS-CoV-2 infection /transmission  and ACE2 expression is demonstrated in gingival and periodontal tissues [3,4].
Gingivitis and periodontitis are two most common forms of inflammatory periodontal diseases (IPDs) and elevated levels of pro-inflammatory cytokines are amongst the most common risk factors for IPDs initiation/progression .
If the intracellular events are similar to those reported in airway epithelial cells , it may be hypothesized that SARS-CoV-2 infection may be involved in pathogenesis IPDs and facilitate periodontal tissues destruction as mentioned on below:
Virus entry to the cell increases ACE2 expression which affects two main genes of RPS3 and SRC in viral replication and inflammatory responses, respectively. As ACE2 overexpression enhances inflammatory responses through greater pro-inflammatory cytokines production, it leads increase binding of SARS-CoV-2. Consequently, negative regulatory activity of ACE2 on angiotensin II may reduce by SARS-CoV-2 resulting an increase in angiotensin II .
In renin-angiotensin system, ACE/Ang II/AT1R axis activates some molecular signaling pathway related to tissue injury including induction inflammatory responses by releasing of cytokines. Oppositely, ACE2/Ang-(1-7)/Mas receptor axis has anti-inflammatory properties. Meanwhile, it seems this axis is an active player in alveolar bone remodeling and its activation can decrease the expression of cytokines directly related to bone resorption .
Since ACE2/Ang-(1-7)/Mas receptor axis is in counter-balanced ACE/Ang II/AT1R axis  downregulation ACE2 by SARS-CoV-2 which may result in an increase of Ang II  enhancing harmful tissue effects of the latter axis.
Although, systemic elevated levels of cytokines can contribute in IPDs onset/exacerbation through enhance the host response to periodontal pathogens . It's pointed out that in COVID-19 patients a higher level of cytokines was observed parallel with the severity of illness  which this may increase probability of IPDs development/progression.
Nevertheless, this hypothesis is theoretically possible but future clinical studies are necessary for confirmation of it.
The author declares that she has no conflict of interest in relation to the publication of this article.
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© The authors, 2020
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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