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Detection of Helicobacter pylori DNA in recurrent aphthous stomatitis tissue by PCR
Author(s) -
Riggio Marcello P.,
Len Alan,
Wray David
Publication year - 2000
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1034/j.1600-0714.2000.291005.x
Subject(s) - polymerase chain reaction , helicobacter pylori , recurrent aphthous stomatitis , etiology , biology , dna extraction , primer (cosmetics) , cancer , genomic dna , nested polymerase chain reaction , gastritis , stomatitis , dna , gene , pathology , gastroenterology , medicine , genetics , chemistry , organic chemistry
Helicobacter pylori is recognised as being an aetiological agent of chronic active gastritis and peptic ulcer disease and has been associated with an increased risk of gastric cancer. The natural reservoir for H. pylori is unknown, although the oral cavity has been the focus of much attention in this respect. Given the histological similarities between gastric and oral ulceration, it seemed prudent to investigate a possible association between H. pylori and recurrent aphthous stomatitis (RAS). In this study, the potential involvement of H. pylori in the aetiology of RAS was investigated using the polymerase chain reaction (PCR). Biopsies from 28 RAS patients were analysed, in addition to 20 oral lichen planus (OLP) and 13 normal biopsies that were used as controls. Genomic DNA was extracted from biopsies, and confirmation of successful extraction of PCR‐amplifiable DNA was achieved by carrying out PCR on each DNA sample with nested primers specific for the human β‐haemoglobin gene. PCR identification of H. pylori was carried out using a primer pair specific for the H. pylori 16S ribosomal RNA (rRNA) gene. Two rounds of PCR were carried out to amplify a 295‐bp product, and the identity of amplified products was confirmed by DNA sequencing. H. pylori DNA was detected in 3 of 28 (11%) RAS samples but not in any of 20 OLP and 13 normal samples. These results do not support a definitive aetiological role for H. pylori in RAS, although the possibility that H. pylori may be involved in a small proportion of RAS cases cannot be excluded.