Review Helicobacter pylori in Tonsillar and Adenoid Tissue and Its Possible Role in Oropharyngeal Carcinogenesis (Helicobacter pylori / carcinogenesis / oropharyngeal carcinoma / tonsillar tissue / adenoid tissue)

Helicobacter pylori is a well-known gastric pathogen. It plays a major role in the pathogenesis of chronic gastritis, duodenal and gastric ulcers, adenocarcinoma and gastric lymphoma. HP infection is one of the most common bacterial infections worldwide. Recently, the oral cavity was proposed as an extragastric reservoir of HP infection. HP was detected by culture and PCR in both dental plaque and saliva. It is supposed that HP infection can cause the same immunological changes in the oropharyngeal mucosa as in gastric mucosa and can also contribute to the progression of oropharyngeal diseases. HP can induce production of different cytokines and regulatory molecules, which are suggested to play a role in carcinogenesis of the oropharynx. Only a few studies have explored the presence of HP in tonsillar and adenoid tissue, where MALT is present similar to the gastric mucosa. The results of these studies were inconsistent. The question of persistence of HP in tonsillar and adenoid tissue and its role in the pathogenesis of oropharyngeal diseases still remains unclear. In this review, recent findings about oral HP are considered. Possibilities of diagnostics of HP in oral specimens are discussed. Introduction Helicobacter pylori (HP) is a spiral, microaerophilic, Gram-negative bacterium. Infection by HP has been established as the major cause of chronic gastritis and plays an important role in the pathogenesis of other gastroduodenal diseases such as peptic ulceration, gastric lymphoma, and gastric cancer (Israel and Peek, 2001). HP is considered to be the most common chronic bacterial infection in humans (Cave, 1996). The prevalence has been estimated to range from 40 to 80 % and it varies widely by geographic area, age, race, ethnicity, and socioeconomic status (Bures et al., 2006). However, the way of its transmission remains unknown. It is supposed that humans represent the only reservoir of HP, which is spread from person to person by oral-oral or faecal-oral route (Brown, 2000). When considering these ways of transmission, it is supposed that HP should be present in the oral cavity. HP was detected in both dental plaque and saliva (Kim et al., 2000). As it was described lately, the presence of HP in gastric mucosa is bound to mucosa-associated lymphatic tissue (MALT) (Cammarota et al., 1997). The same tissue is located in the oral cavity and pharynx in Waldayer’s circuit. For this reason, great interest has recently been focused on detection of HP presence in tonsillar and adenoid tissue.