Oral Viral Load of Sars-Cov-2 and Exacerbation of Chronic Periodontal Disease in Patients With Novel Coronavirus Infection (Covid-19)

Object. SARS-CoV-2 is a coronavirus that causes the acute respiratory infection novel coronavirus infection (COVID-19). Cells expressing ACE 2 (angiotensin converting enzyme 2) receptors, which are present in many organs and tissues of humans, including the epithelium of the nose and mouth, are susceptible to SARS-CoV-2. At the same time, hyperinflammation is characteristic of novel coronavirus infection (COVID-19), with a massive production of cytokines — the so-called cytokine storm [1]. Periodontal tissues are also highly sensitive to such hyperinflammatory reactions, which makes it possible to initiate an exacerbation of chronic periodontal pathology. Objective: To determine the relationship between SARS-CoV-2 oral reproduction and exacerbation of chronic periodontal disease in patients with novel coronavirus infection (COVID-19). Material and methods. Study of 18 patients of the COVID-hospital (Kazan), who are undergoing hospital treatment with a diagnosis of novel coronavirus infection (COVID-19)/community-acquired pneumonia, was carried out. To test SARS-CoV-2, material was sampled with special sterile swabs and pins from the nasopharynx, periodontal pocket and tongue surface (respectively). The method of polymerase chain reaction with reverse transcription (RT-PCR) was used. Results. SARS-CoV-2 RNA was not detected in biomaterials from the nasopharynx, periodontal pocket and tongue surface 94.4% of patients with confirmed with new coronavirus infection (COVID-19) during acute inflammation (community-acquired pneumonia). At the same time, clinical examination showed that exacerbation of chronic generalized periodontitis was diagnosed in 100% of patients. Conclusion. It is most likely that the exacerbation of chronic generalized periodontitis in patients with novel coronavirus infection (COVID-19) is not associated with the reproduction of SARS-CoV-2 in the oral cavity, but is a consequence of hyperactivation of immune and inflammatory defense mechanisms.