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medrxiv; 2022.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2022.03.10.22271304

ABSTRACT

Objective Chronic periodontitis has been proposed to be linked to coronavirus disease (COVID-19) on the basis of itsinflammation mechanism. We aimed to evaluate this association by investigating the expression of Angiotensin Converting Enzyme-2 (ACE2) in periodontal compartments, which contain dysbiosis-associated pathogenic bacteria, and how it can be directly or indirectly involved in exacerbating inflammation in periodontal tissue. Material and Methods This observational clinical study included 23 adult hospitalized patients admitted to Universitas Indonesia Hospital with PCR-confirmed COVID-19, while 6 non-COVID-19 participants come to periodontal clinic were included as control. Using real time-PCR (qPCR) and gingival crevicular fluids (GCF) samples from COVID-19 patients with and without diabetes and periodontitis, we assessed the mRNA expression of angiotensin-converting enzyme 2 (ACE2), IL-6, IL8, complement C3, and LL37 as well as the relative proportion of Porphyromonas gingivalis , Fusobacterium nucleatum , and Veillonella parvula to represent the dysbiosis condition in periodontal microenvironment. All analyses were performed to determine their relationship. Results ACE2 mRNA expression was detected in the GCF of periodontitis-COVID-19 patients with and without diabetes. However, only periodontitis-COVID-19 patients with diabetes showed a positive relationship between ACE2 expression and inflammatory conditions in the periodontal microenvironment. In addition, the interplay between pro-inflammatory cytokine (Il-6) and complement C3 could be used as a predictor of the severity of periodontal inflammation in COVID-19 patients with diabetes. Conclusion The study data show that the SARS-CoV-2 entry gene is expressed in the GCF of patients with COVID-19, and its expression correlates with inflammatory markers.


Subject(s)
Coronavirus Infections , Periodontitis , Chronic Periodontitis , Diabetes Mellitus , COVID-19 , Dysbiosis , Inflammation
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