BACKGROUND: An oral-to-oral route of transmission of Helicobacter pylori infection has been postulated, which is supported by the observation that H. pylori is present in the saliva and in dental plaque. On the basis of this assumption, an increased risk of H. pylori infection among dentists was postulated. METHOD: Serum and salivary H. pylori immunoglobulin (lg)G antibodies were measured in a group of practising dentists. For comparison we also studied a group of controls from the same urban area matched for age, sex, smoking habits, alcohol and non-steroidal anti-inflammatory drug consumption, and history of dyspepsia. RESULTS: There was no significant difference in serum H. pylori lgG antibodies titres between dentists and controls [optical density (OD) 0.991 +/- 0.588 versus 1.025 +/- 0.591, respectively]. Salivary H. pylori lgG were 0.693 +/- 0.726 and 0.661 +/- 0.614 OD in the dentists and control groups, respectively. The frequency of H. pylori-seropositive subjects did not differ between the two groups [22 out of 39 (56%) versus 46 out of 71 (64%)]. A positive saliva assay was found in 23 out of 39 (59%) dentists and in 44 out of 71 (62%) controls. The odds ratio for a dentist being H. pylori-positive was 0.7 (95% confidence interval 0.3-1.7) by serology and 0.9 (95% confidence interval 0.4-2.1) by salivary antibody assay. CONCLUSION: The data of this study do not support the concept that dentists are a high-risk group for H. pylori infection.
BACKGROUND: An oral-to-oral route of transmission of Helicobacter pylori infection has been postulated, which is supported by the observation that H. pylori is present in the saliva and in dental plaque. On the basis of this assumption, an increased risk of H. pyloriinfection among dentists was postulated. METHOD: Serum and salivary H. pylori immunoglobulin (lg)G antibodies were measured in a group of practising dentists. For comparison we also studied a group of controls from the same urban area matched for age, sex, smoking habits, alcohol and non-steroidal anti-inflammatory drug consumption, and history of dyspepsia. RESULTS: There was no significant difference in serum H. pylori lgG antibodies titres between dentists and controls [optical density (OD) 0.991 +/- 0.588 versus 1.025 +/- 0.591, respectively]. Salivary H. pylori lgG were 0.693 +/- 0.726 and 0.661 +/- 0.614 OD in the dentists and control groups, respectively. The frequency of H. pylori-seropositive subjects did not differ between the two groups [22 out of 39 (56%) versus 46 out of 71 (64%)]. A positive saliva assay was found in 23 out of 39 (59%) dentists and in 44 out of 71 (62%) controls. The odds ratio for a dentist being H. pylori-positive was 0.7 (95% confidence interval 0.3-1.7) by serology and 0.9 (95% confidence interval 0.4-2.1) by salivary antibody assay. CONCLUSION: The data of this study do not support the concept that dentists are a high-risk group for H. pyloriinfection.