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 un
known, although the oral cavity has been the focus of much attention in thi
s respect. Given the histological similarities between gastric and oral ulc
eration, it seemed prudent to investigate a possible association between H,
pylori and recurrent aphthous stomatitis (RAS). In this study, the potenti
al involvement of H. pylori in the aetiology of RAS was investigated using
the polymerase chain reaction (PCR). Biopsies from 28 RAS patients were ana
lysed, in addition to 20 oral lichen planus (OLP) and 13 normal biopsies th
at were used as controls. Genomic DNA was extracted from biopsies, and conf
irmation of successful extraction of PCR-amplifiable DNA was achieved by ca
rrying out PCR on each DNA sample with nested primers specific for the huma
n beta-haemoglobin gene. PCR identification of H. pylori was carried out us
ing 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 id
entity 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 invol
ved in a small proportion of RAS cases cannot be excluded.