Rck. Jordan et al., ABSENCE OF HELICOBACTER-PYLORI DNA IN SALIVARY LYMPHOEPITHELIAL LESIONS, Journal of oral pathology & medicine, 26(10), 1997, pp. 454-457
Helicobacter pylori is a common cause of chronic gastritis and has bee
n implicated as the main agent responsible for the development of lymp
homas of mucosa associated lymphoid tissue (MALT) in the stomach. An u
ncommon cause of salivary gland swelling is salivary lymphoepithelial
lesion (SLEL), which shows histological features of aquired MALT and i
s associated with the development of MALT-type lymphomas. Since H. pyl
ori has been identified in the oral cavity, we hypothesised that this
organism might act as a potential antigen for the development of MALT
in salivary glands. Routinely processed biopsies of 20 SLEL were scree
ned for H. pylori DNA using a sensitive two-stage PCR technique to amp
lify the 16S ribosomal RNA gene. Immunoglobulin heavy chain gene monoc
lonality was determined by amplifying the VDJ gene using a nested PCR
technique. All SLEL had histological features of organised MALT and 14
cases showed Ig heavy chain gene monoclonality consistent with MALT l
ymphoma. None of the SLEL contained H. pylori DNA. In contrast to the
putative role of H. pylori as an antigenic stimulus in gastric MALT ly
mphomas, it appears not to play a role locally in the development of M
ALT or MALT lymphomas of the salivary gland.