COVID-19 and Oral Mucosal Lesions: a Systematic Review.

Introduction: COVID-19 disease is caused by a mutated strain of the coronavirus family "SARS-CoV-2". It affects especially the respiratory system, but many clinical manifestations outside this system have been reported. Oral manifestations are uncommon, however, with the absence of common signs, they may represent the onset of COVID-19 disease. The aim of this systematic review is to observe if there is a correlation between SARS-CoV-2 infection and oral manifestations. Methods: The research was conducted on PubMed, Scopus, Google Scholars and Cochrane Library from March 2020 to May 2023. Each study was subjected to data extraction; including authors, year and month of publication, study type, patients' average age, type and localization of oral lesions, the positivity of the SARS-CoV-2 virus test, and comorbidities. Results: A total of 43 studies met the inclusion criteria and a total of 507 COVID-19 patients with 496 oral lesions were included. The most frequent was ulceration and the most common localization was the tongue. Conclusions: The results of our systematic review show a possible correlation between COVID-19 infection and oral manifestations. Further studies are required to determine if the lesions are directly connected to the virus.

Comparison of the effects of PRKAR1A and PRKAR2B depletion on signaling pathways, cell growth, and cell cycle control of adrenocortical cells.

The cyclic AMP/protein kinase A signaling cascade is one of the main pathways involved in the pathogenesis of adrenocortical tumors. The PKA R1A and R2B proteins are the most abundant regulatory subunits in endocrine tissues. Inactivating mutations of PRKAR1A are associated with Carney complex and a subset of sporadic tumors and the abundance of R2B protein is low in a subset of secreting adrenocortical adenomas. We previously showed that PRKAR1A and PRKAR2B inactivation have anti-apoptotic effects on the adrenocortical carcinoma cell line H295R. The aim of this study was to compare the effects of PRKAR1A and PRKAR2B depletion on cell proliferation, apoptosis, cell signaling pathways, and cell cycle regulation. We found that PRKAR2B depletion is compensated by an upregulation of R1A protein, whereas PRKAR1A depletion has no effect on the production of R2B. The depletion of either PRKAR1A or PRKAR2B promotes the expression of Bcl-xL and resistance to apoptosis; and is associated with a high percentage of cells in S and G2 phase, activates PKA and MEK/ERK pathways, and impairs the expression of IkB leading to activate the NF-κB pathway. However, we observed differences in the regulation of cyclins. The depletion of PRKAR1A leads to the accumulation of cyclin D1 and p27kip, whereas the depletion of PRKAR2B promotes the accumulation of cyclin A, B, cdk1, cdc2, and p21Cip. In conclusion, although the depletion of PRKAR1A and PRKAR2B in adrenocortical cells has similar effects on cell proliferation and apoptosis; loss of these PKA subunits differentially affects cyclin expression.