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Although coronavirus disease 2019 (COVID-19) vaccines exhibit diverse side effects, taste and saliva secretory disorders have remained poorly understood despite their negative impact on the overall quality of life. The present study aimed to characterize oral adverse effects following COVID-19 vaccination and assess their similarities with oral symptoms in COVID-19 patients. A literature search was conducted in databases, including PubMed, LitCovid, and Google Scholar, to retrieve relevant studies. The narrative review indicated that a certain number of vaccinated people develop ageusia, dysgeusia, hypogeusia, xerostomia, and dry mouth, while they are rare compared with COVID-19 oral symptoms. The prevalence of oral adverse effects varies by country/region and such geographical differences may be related to the type of vaccine used. Similar to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, COVID-19 vaccination adversely affects taste perception and salivary secretion in females and older subjects more frequently than in males and younger subjects. Their impairments mostly appear within 3 days of vaccination, and bitter taste is specifically impaired in some cases. Considering that oral adverse effects following COVID-19 vaccination share some characteristics with oral symptoms in COVID-19 patients, it is speculated that the spike protein derived from COVID-19 vaccination and SARS-CoV-2 infection may be pathophysiologically responsible for taste and saliva secretory disorders. This is because such spike protein has the potential to interact with ACE2 expressed on the relevant cells, produce proinflammatory cytokines, and form antiphospholipid antibodies. Our results do not deny the advantages of COVID-19 vaccination, but attention should be paid to post-vaccination oral effects in addition to COVID-19 oral symptoms. [ABSTRACT FROM AUTHOR]

Dental professionals routinely work in proximity to patients even when either or both of them have suspected or confirmed COVID-19. The oral cavity also serves as a reservoir for SARS-CoV-2 because the virus is present in and replicates in oral secretions (saliva and gingival crevicular fluid), oral tissues (salivary gland and periodontal tissue), and oral microenvironments (gingival sulcus and periodontal pocket). Despite a high risk of SARS-CoV-2 infection, the prevalence of COVID-19 in dentists, dental hygienists, dental assistants, and their patients was similar to that in the general population even during the pandemic. We propose that eugenol, which is responsible for the ambient odor specific to dental offices, could contribute to prevention of COVID-19 in dental settings. Eugenol is not only released from dental materials (filling, cement, and sealer) but is also aerosolized by dental procedures (grinding, polishing, and restoration). Such eugenol has been suggested to possess the potential to inhibit the infectivity and replication of SARS-CoV-2, the entry of SARS-CoV-2 into human cells by binding specifically to the viral spike protein, and the protease indispensable for SARS-CoV-2 replication. It has been shown that aerosolized eugenol acts on airborne viruses to reduce their loads. This review highlights a hypothesis that the environment of dental offices impregnated with eugenol suppresses SARS-CoV-2 airborne transmission and SARS-CoV-2 contagion between dental professionals and patients, preventing COVID-19 in dental practice. Anti-COVID-19 eugenol might give insights into the safe delivery of dental treatment and oral care in the COVID-19 era. Highlights of the Study: Despite a high risk of infection with severe acute respiratory syndrome coronavirus 2, the prevalence of coronavirus disease 2019 in dental professionals and patients was not high even during the pandemic. Eugenol, which is released from dental materials and aerosolized by dental procedures, has the ability to inhibit viral infectivity, replication, and cellular entry. We propose that eugenol prevents coronavirus disease 2019 in dental practice. [ABSTRACT FROM AUTHOR]

Diverse manifestations have been recognized to last for a long time in patients infected with SARS-CoV-2. However, understanding of oral sequelae after recovery from COVID-19 is relatively poor compared to that of oral symptoms in the acute phase of COVID-19 and other COVID-19 sequelae. The aim of the present study was to characterize persistent gustatory and saliva secretory dysfunctions and to speculate on their pathogenic mechanisms. Articles were retrieved by searching scientific databases with a cutoff date of September 30, 2022. The literature search indicated that ageusia/dysgeusia and xerostomia/dry mouth are reported by 1–45% of COVID-19 survivors at follow-ups of 21–365 days and by 2–40% of COVID-19 survivors at follow-ups of 28–230 days, respectively. The prevalence of gustatory sequelae partly depends on difference in ethnicity, gender, age, and disease severity of subjects. Co-occurring gustatory and saliva secretory sequelae are pathogenically related to either or both of the following: expression of SARS-CoV-2 cellular entry-relevant receptors in taste buds and salivary glands, and SARS-CoV-2 infection-induced deficiency in zinc that is essential for normality of taste perception and saliva secretion. Given the long-term oral sequelae, hospital discharge is not the end of the disease; therefore, careful attention should be continuously paid to oral conditions of post-COVID-19 patients. [ABSTRACT FROM AUTHOR]

Objective: Although acetaminophen is one of the most widely used over-the-counter drugs, the mechanisms by which this classical drug exerts analgesic, hepatotoxic, and nephrotoxic effects remain unclear. We hypothesized that acetaminophen might act on cellular membranes of nerves, liver, and kidneys. In order to verify this hypothesis, we studied the interactivity of acetaminophen with biomimetic lipid bilayer membranes by comparing with structurally related phenacetin.Methods: Liposomal membranes (unilamellar vesicles suspended in the buffer of pH 7.4) were prepared with phospholipids and cholesterol to mimic the membrane lipid composition of neuronal cells, hepatocytes, and nephrocytes. They were subjected to reactions with acetaminophen and phenacetin at clinically relevant concentrations, followed by measuring fluorescence polarization to determine their membrane interactivity to modify membrane fluidity.Results: Acetaminophen and phenacetin interacted with neuro-mimetic and hepato-mimetic membranes to increase membrane fluidity at 10-100 μM. Both drugs were more effective in fluidizing hepato-mimetic membranes than neuro-mimetic membranes. Although the relative membrane-interacting potency was phenacetin >> acetaminophen in neuro-mimetic and hepato-mimetic membranes, such membrane effects conflicted with their relative analgesic and hepatotoxic effects. Acetaminophen and phenacetin strongly interacted with nephro-mimetic membranes to increase membrane fluidity at 2-100 μM and 0.1-100 μM, respectively. Phenacetin interacted significantly with nephro-mimetic membranes at lower concentrations (<2 μM) than acetaminophen, which was consistent with their relative nephrotoxic effects.Conclusion: In comparison with phenacetin, lipid composition-dependent membrane interactivity of acetaminophen could be related to nephrotoxicity but not to analgesic activity and hepatotoxicity. [ABSTRACT FROM AUTHOR]