Expression of Salivary Ceramide Synthase 1 (CERS1) in Recurrent Aphthous Stomatitis (RAS): A Cross-Sectional Institutional Study

唾液神经酰胺合酶 1 (CERS1) 在复发性口疮性口炎 (RAS) 中的表达:一项横断面机构研究

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作者:Sangamithra Surendran, Pratibha Ramani, Karthikeyan Ramalingam, Selvaraj Jayaraman

Abstract

Background The increased rate of apoptosis is one of the major causes of ulcer formation. A variety of factors can influence the rate of apoptosis. Ceramide (CER) is one such factor that has been proposed to play a role in signaling apoptosis induced by extracellular agents. Recurrent aphthous stomatitis (RAS) is a common condition that initially presents in children or adolescents. Multiple recurrent small, round, or ovoid ulcers with erythematous haloes and circumscribed margins are its characteristic features. Its pathogenesis is still a mystery. Ceramide synthase 1 (CERS1) aids in the production of C18 CER. Although the role of CERS1 in aphthous is well understood, its possible intricate role in pathogenesis remains unknown. Aim To evaluate the expression of salivary CERS1 in patients with RAS and healthy individuals. Materials and methods 30 patients were included in the present study. Ethical clearance for this study was obtained, and there were no gender or age limits for enrollment. After obtaining informed consent, 30 salivary samples were collected from patients with RAS (n=15) and from healthy individuals (n=15). Enzyme-linked immunosorbent assay (ELISA) was performed using the CERS1 kit by MyBioSource Inc (San Diego, USA) and the results were recorded. The Chi-square test and Independent t-test were used for statistical analysis with SPSS v23.0 (IBM, Chicago, USA) with a significant p-value of <0.05. Results CERS1 expression was identified in the saliva of all participants. There was a decrease in the salivary CERS1 level in RAS patients (7.6 +/- 2.0 pg/ml) when compared to healthy individuals (8.3 +/- 1.8 pg/ml) but it did not achieve statistical significance. Conclusion We found that salivary CERS1 levels decreased in RAS patients. More research is required to understand CERS1's pathogenetic role.

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