Can Helicobacter pylori be one of the etiological factors of oropharyngeal carcinogenesis?

Overview

Helicobacter pylori (HP) is a well known gastric pathogen. It plays a major role in the pathogenesis of chronic gastritis, duodenal and gastric ulcers, adenocarcinoma, gastric MALT lymphoma and a number of other diseases. HP infection is the most common bacterial infection worldwide. Recent studies have explored the relationship between HP and the oral cavity. The upper aerodigestive tract could be directly exposed to the bacterium by gastroesophageal reflux (GER). It is supposed that HP infection could cause the same immunological changes in the oropharyngeal mucosa as in gastric mucosa, and contribute to the progression of oropharyngeal diseases. HP can induce the production of different cytokines and regulatory molecules, which could promote carcinogenesis (e.g. spinocellular carcinoma) of the oropharynx. Some studies have confirmed presence of HP in dental plaque. Only a few studies have explored the presence of HP in tonsilar tissue, where mucosa associated lymphatic tissue (MALT) is present similarly as in gastric mucosa. The results of these studies were inconsistent. The question of persistence of HP in tonsilar tissue and its role in the pathogenesis of oropharyngeal diseases still remains unclear.

Key words:
Helicobacter pylori, spinocellular carcinoma, NO synthase, Epithelial Growth Factor – EGF, Transforming Growth Factor –TGF