• AHMED MOHAMMED SALIH Assis. Professor, Duhok Medical research center, College of Medicine, University of Duhok, Kurdistan Region, Iraq.
  • NAZDAR M. OMER Assis. Lecturer, Department of Medical Physiology and Pharmacology, College of Medicine, University of Duhok, Kurdistan Region, Iraq.
  • ABDULRAZZAQ M Dentist, Duhok Dentistry Center, Duhok, Kurdistan Region, Iraq.
Keywords: cagA, dupA, Helicobacter pylori, Recurrent aphthous stomatitis, vacA


Background: Recurrent Aphthous Stomatitis (RAS) is an inflammatory condition of unknown etiology characterized by recurrent and painful lesions, with single or multiple ulcerations that are confined to the oral cavity mucosa. The current study aimed at the molecular detection of oral H. Pylori and its vacA, cagA, and dupA virulence genes in patients with Recurrent Aphthous Stomatitis in Duhok, Kurdistan Region, Iraq.

Method: This is a cross-sectional study. It has been conducted in the laboratories of the college of medicine, Duhok city, Kurdistan Region, Iraq. A total of ninety-two individuals were included in the present study; forty-six patients with RAS consisted of 11 females and 35 males and forty six apparently healthy individuals as control group composed of 23 females and 23 males. A swab was taken from the RAS lesion of each in the patients' group and the control group's oral cavity (cheek) and submitted to a conventional PCR-based assay to detect the H. Pylori DNA using specific primers targeting 16SrRNA gene. The family history for RAS of both the patients and the control group was investigated. H. pylori virulence genes vacA, dupA, and cagA(m1) were investigated in all extracted DNA samples using specific primers.

Results: H. Pylori DNA was detected only in 2 (4.34%) of the patients and one (2.17%) of the control group. The family history of RAS disease was positive in 24 (52.17%) of the cases, while only one individual (2.173%) of the control group had a positive family history of RAS disease. One of the H. pylori positive RAS patients showed a positive result for the three vacA, dupA, and cagA(m1) virulence genes, whereas the other one was positive for only dupA and cagA(m1) virulence genes. In addition, the H. pylori positive healthy control showed a positive result for all the three vacA, dupA, and cagA(m1) virulence genes.

Conclusion: There was no significant attribution H. Pylori in the etiology of RAS, while there was a highly significant relation of recurrent RAS with the family history of the patients (p < 0.01).


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