Impact of SARS-CoV-2 on oral health

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak in Wuhan, China, was first reported on December 31^st, 2019. These initial coronavirus disease 2019 (COVID-19) cases caused by SARS-CoV-2 were linked to an animal wet market.

Similarities between SARS-CoV-2 and other coronaviruses suggest that bats may be natural hosts and potential reservoirs for this virus, which were transmitted to humans. New research, published in the journal Biomedicines, discusses SARS-CoV-2 and its impact on oral health.

Study: SARS-CoV-2: Overview and Its Impact on Oral Health. Image Credit: Andrii Vodolazhskyi/Shutterstock

Airborne transmission of COVID-19 infection

SARS-CoV-2 spreads through droplet transmission; airborne transmissions through aerosols have also been documented. This infection is highly contagious and can also be transmitted via the oral-fecal route or through contacting infected surfaces or oral fluids. Therefore, dentists and other healthcare professionals are at high risk for COVID-19 infections.

In addition, several dental and medical procedures generate aerosols. Hence, dental and medical offices tend to propagate cross-infection among patients and healthcare professionals. SARS-CoV-2 has a single-stranded RNA with cell-surface spike glycoproteins. These facilitate adherence and penetration of the virus into the host cells. The main cellular receptor for the spike glycoprotein is the angiotensin-converting enzyme 2 (ACE2), which is found in the lungs, kidneys, myocardial cells, salivary glands, and tongue.

COVID-19 can progress in three main stages – stage 1 involves the activation of innate immunity; stage 2 involves the activation of adaptive immunity, and stage 3 involves cytokine release syndrome or the “cytokine storm”.

The cytokine storm – an exaggerated cytokine release by a hyper-responsive host, is characterized by hyper-coagulability, dysfunction of multiple organs, acute lung injury, and shock. This exaggerated reaction can render potential immunodeficiency states.

Periodontal inflammation is likely to influence COVID-19 susceptibility and pathogenesis. The early mucosal immune response is dominated by immunoglobulin A (IgA). Individuals with prior SARS-CoV-2 virus exposure appear to have high levels of neutralizing secretory antibodies.

Long COVID or post-COVID-19 syndrome can develop when SARS-CoV-2 symptoms persist beyond four weeks after a confirmed diagnosis. Emerging evidence suggests that patients may continue to suffer from persistent psychiatric or neurological symptoms six months following the disease onset. Long COVID is more common among the younger age groups. Meanwhile, elderly and immunocompromised individuals are more vulnerable to severe symptoms and exhibit earlier waning of vaccine effectiveness.

The ACE2 receptors are present in tissues of the floor of the mouth, tongue, buccal mucosa, and gingiva while oral ACE2-positive cells reside mainly in the taste organs. In the early stage of COVID-19, the virus is detected in saliva as ACE2-positive salivary glands are also targets for SARS-CoV-2, which may affect salivary gland function. Thus, COVID-19 can result in a dry mouth.

Salivary glands harbor a greater number of ACE2 receptors than the lungs, and thus, could act as a reservoir for SARS-CoV-2 in asymptomatic patients. The ACE2 receptors are also present in fibroblasts of the periodontium; elevated protease levels due to chronic periodontitis can increase the risk for viral entry. The viral fusion to the host cells requires cleavage of the SARS-CoV-2 S protein by transmembrane protease serine 2 (TMPRSS2) or furin, and pathogenic bacteria found in the oral cavity can also cleave the S protein of SARS-CoV-2.

Therefore, oral health could act as a major determining factor for COVID-19 susceptibility. Poor oral hygiene and periodontitis can render dysbiotic biofilms that promote cytokine release. This may result in pro-inflammatory systemic effects and could promote the spread of pulmonary infections. Furthermore, the exchange of pathogenic bacteria from the oral cavity to the lung may directly cause lung infections.

Moreover, aspirated pathogenic bacteria may cause inflammation of the lower respiratory tract may predispose to secondary bacterial infections in COVID-19 patients. In patients with comorbidities and the elderly, the increased risk of bacterial aspiration due to a poor swallowing reflex may lead to a higher preponderance to severe COVID-19 disease with bacterial superinfection.

Poor oral hygiene in relation to COVID-19

Poor oral hygiene increases periodontal pathogens. These pathogens have been detected in the lower respiratory tracts of COVID-19 patients. These bacteria can also degrade the S protein of SARS-CoV-2, enhancing its penetration and infectivity. Additionally, the lack of proper oral care in COVID-19 patients, especially among those hospitalized for prolonged periods, may increase the risk of aspirated pathogenic oral bacteria and inflammation of the lower respiratory tract.

Emerging evidence suggests that COVID-19 patients with periodontal disease have a higher mortality risk than those without. This is because poor oral hygiene and periodontitis promote the progression of COVID-19 via upregulation of ACE2 and proinflammatory cytokines. Thus, management and control of periodontitis may reduce or minimize the risk of SAR-CoV-2 infections.

Oral antiseptics used as pre-procedural rinses can aid in preventing cross-infection and the number of bacteria in aerosols. The effectiveness of pre-procedural mouth rinses in reducing the number of aerosolized microbes during dental treatment has been documented.

Oral antiseptics can reduce viral load and disease transmission, by disrupting the viral lipid envelope; the ones being used are – 1% povidone-iodine; 0.05-0.10% cetylpyridinium chloride; 0.12% chlorhexidine; 1% hydrogen peroxide; beta-cyclodextrin with citrox; and essential oil mouth rinses, such as – eucalyptol, thymol, menthol, and methyl salicylate.

A combination of two mouth rinses – 1% hydrogen peroxide and 0.2-0.3% chlorhexidine, can also be advantageous and can provide a dual mechanism of action. These antiseptic rinses can decrease the salivary viral load and reduce the risk of SARS-CoV-2 dissemination.

Gargling with antimicrobial mouthwashes or the use of antimicrobial nasal sprays in suspected or confirmed COVID-19 patients may inhibit transmission of infection and protect healthcare providers. While optimal oral hygiene and treatment of periodontal disease can reduce ACE2 expression, inflammatory cytokines and may aid in the prevention of aspiration pneumonia. Therefore, maintaining periodontal health may reduce host susceptibility to COVID-19 and may prevent COVID-19 aggravation.

In addition, periodontal therapy also improves systemic diseases such as COPD and diabetes; maintenance of dental health may reduce mortality and morbidity through lowering host susceptibility to COVID-19 aggravation.

Conclusion

Periodontal health and good oral hygiene are crucial to maintaining overall health and help in survival against SARS-CoV-2 and for preventing COVID-19 aggravation. The use of antimicrobial mouth rinses may be incorporated in routine practice used to enhance oral health and to inhibit the transmission of COVID-19 in the dental office.