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Published on: April 1, 2019
Association of cell adhesion molecule gene polymorphisms with recurrent aphthous stomatitis
Asem Alkhateeb1, Jumana Karasneh, Hebah Abbadi
1Department of Biotechnology and Genetics, Jordan University of Science and Technology (JUST), Irbid, Jordan.
Genetic variations in E-selectin rs5361 are linked to recurrent aphthous stomatitis (RAS) susceptibility. This study identifies specific E-selectin genotypes as potential risk factors for developing this common oral condition.
Area of Science:
- Genetics
- Immunology
- Oral Medicine
Background:
- Recurrent aphthous stomatitis (RAS) is a prevalent oral ulcerative condition.
- Adhesion molecules like VCAM-1, E-selectin, and ICAM-1 are upregulated at ulcer sites, potentially promoting leukocyte infiltration.
- Gene polymorphisms in these adhesion molecules may influence RAS susceptibility.
Purpose of the Study:
- To investigate the association between specific gene polymorphisms in selectins, ICAM, and VCAM and the susceptibility to RAS.
- To identify potential genetic markers for RAS risk.
Main Methods:
- Genotyping of six single nucleotide polymorphisms (SNPs) in E-selectin, L-selectin, ICAM-1, ICAM-5, and VCAM-1 genes in 96 RAS cases and 153 controls from Jordan.
- Statistical analysis including chi-square and logistic regression to determine associations.
- Haplotype analysis using EH and Phase 2.1 programs.
Main Results:
- A significant association was found between the E-selectin rs5361 gene polymorphism (A allele, AA and AC genotypes) and increased RAS risk (Pcorr = 0.027).
- The TAA haplotype (rs2205849, rs5361, rs1805193) also showed a significant association with RAS (P = 0.03).
- No significant associations were observed for other tested SNPs.
Conclusions:
- This study provides the first evidence linking E-selectin rs5361 A allele and AA/AC genotypes to an elevated risk of recurrent aphthous stomatitis.
- Further research in diverse populations and functional studies are recommended to validate these findings and elucidate the underlying biological mechanisms.
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