SARS-CoV-2 Infection and Oral Health: Therapeutic Opportunities and Challenges

Abstract

The novel corona virus, Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and the disease it causes, COVID-19 (Coronavirus Disease-2019) have had multi-faceted effects on a number of lives on a global scale both directly and indirectly. A growing body of evidence suggest that COVID-19 patients experience several oral health problems such as dry mouth, mucosal blistering, mouth rash, lip necrosis, and loss of taste and smell. Periodontal disease (PD), a severe inflammatory gum disease, may worsen the symptoms associated with COVID-19. Routine dental and periodontal treatment may help decrease the symptoms of COVID-19. PD is more prevalent among patients experiencing metabolic diseases such as obesity, diabetes mellitus and cardiovascular risk. Studies have shown that these patients are highly susceptible for SARS-CoV-2 infection. Pro-inflammatory cytokines and oxidative stress known to contribute to the development of PD and other metabolic diseases are highly elevated among COVID-19 patients. Periodontal health may help to determine the severity of COVID-19 infection. Accumulating evidence shows that African-Americans (AAs) and vulnerable populations are disproportionately susceptible to PD, metabolic diseases and COVID-19 compared to other ethnicities in the United States. Dentistry and dental healthcare professionals are particularly susceptible to this virus due to the transferability via the oral cavity and the use of aerosol creating instruments that are ubiquitous in this field. In this review, we attempt to provide a comprehensive and updated source of information about SARS-CoV-2/COVID-19 and the various effects it has had on the dental profession and patients visits to dental clinics. Finally, this review is a valuable resource for the management of oral hygiene and reduction of the severity of infection.

Keywords: Angiotensin Converting Enzyme 2 (ACE-2); COVID-19; dental practice; inflammation; oxidative stress; periodontitis; saliva.

Figure 1

Cumulative confirmed cases of COVID-19 in United States as of November 4, 2020. The number of confirmed COVID-19 deaths by age (A) [12], and the number of confirmed COVID-19 deaths by race and ethnicity (B) [22] are presented.

Figure 2

An overview of COVID-19 infection. COVID-19 infection is more pronounced in populations with comorbidities such as periodontitis, obesity, diabetes and cardiovascular disease. COVID-19 infection induces oxidative stress, triggers unregulated cytokine production (cytokine storm) and inflammation [89,90,91]. These events enhance the risk of morbidity and mortality rate in most vulnerable populations [21,23].

Figure 3

Schematic representation of the proposed mechanism involved in COVID-19-infection inducing multiple organ failure. Binding of viral protein to Angiotensin Converting Enzyme 2 (ACE-2) leads to virus entry. ACE-2 gene expression in oral tissues [46,47], lungs [48,49], vascular [71], kidney [50], stomach [51], and colon [52] has been shown to repress nuclear factor erythroid 2–related factor 2 (NRF2) [53]. A possible mechanism of ACE-2 and reactive oxygen species (ROS) activation by COVID-19 and the repressing of NRF2 executes oral manifestations, acute respiratory distress syndrome (ARDS) in lungs, inflammation and oxidative stress in multiple organs. Suppression of estrogen receptors (ER) by COVID-19 infection elevates inflammation in multiple organs. Suppression of NRF2 by COVID-19 infection reduces tetrahydrobiopterin (BH_4, a cofactor for nitric oxide synthase) availability, nitric oxide synthases (NOS) uncoupling, thus altering overall gastrointestinal (GI) function.