Absence of Helicobacter pylori in the oral cavity of 10 non‐dyspeptic subjects demonstrated by real‐time polymerase chain reaction

Abstract

Helicobacter pylori is a gram-negative, curved, microaerophilic organism that has been implicated in the aetiology of gastritis, in the process of gastric and duodenal ulcer formation, and in gastric cancer (15,17). Approximately 10% of individuals are affected by gastritis and/or gastric ulcer during their lifetime and over 50% of the world's population carries this infection (7). The prevalence of gastric H. pylori infection depends on age and varies strongly between developing and developed countries, and according to ethnicity, place of birth and socioeconomic factors among people living in the same country Background/aims: Helicobacter pylori plays a significant role in gastric disease. However, the presence of this bacterium in the oral cavity remains controversial. The aim of the present study was to detect and quantify H. pylori in 29 different sites of the oral cavity in non-dyspeptic subjects by means of real-time polymerase chain reactions (PCR). Methods: Ten subjects without gastric symptoms were studied. Samples from unstimulated saliva, three sites of the tongue, oral mucosa, and 12 sites of both supragingival and subgingival plaque were collected from each subject. DNA was extracted from the oral samples and analysed for the presence of H. pylori by real-time PCR (LightCycler Ò ) using JW23/22 primers which targeted the 16S rRNA gene. DNA from H. pylori DSM 4867 was used as a positive control. Relative quantification with external standards was performed by calculating the target to reference ratio. Results: Amplification efficiency for the LightCycler Ò 2.0 runs ranged from 1.8 to 2.4. Melting curve analysis identified all the positive control capillaries, which contained H. pylori reference DNA, as a single and narrow peak at a melting temperature between 84.5 and 84.9°C. All the negative control capillaries with no template control and the 29 oral samples from each subject showed either no melting peaks or broad melting peaks below 80°C, which were considered as primer dimers. Therefore, H. pylori was not detected from any of the 290 oral samples. Conclusion: Helicobacter pylori seems not to be permanently present in the oral cavity of a non-dyspeptic population.

Detection of Helicobacter Pylori using PCR in dental plaque of patients with and without gastritis

“…Also they did not find any association between H.pylori in dental plaque and stomach which is not in agreement with our study. Martinez-Gomis et al (15) found no H. pylori in the dental plaque of non-gastritis patients that supports our findings. Gebara et al (16) (20).…”

The investigation of Helicobacter pylori in the dental biofilm and saliva samples of children with dyspeptic complaints

“…In studies in which H.pylori was detected in dental biofilm and saliva with RT-PCR, Burgers et al [3], Altındiş et al [55], Sayed et al [69] and Martinez-Gomis et al [70] used adults as the subjects, Bharath et al [71] completed their studies using with adults and children. Investigations conducted by, Valdez-Gonzales et al [5] and Ou et al [72] involved the use of only children.…”

Lack of Association Between Helicobacter pylori Infection and Oral Lichen Planus

“…However based on some evidence oral cavity can be considered a reservoir for H. pylori in non-dyspeptic individuals, some researchers believe in temporary presence of H. pylori in such situation (Martinez-Gomis et al, 2006;Burgers et al, 2008). Other researchers believe that non-infectious H. pylori might exist in the oral cavity which is just able to form colonies and invade tissues under special conditions such as concomitant infections (Martinez-Gomis et al, 2006).…”

“…Other researchers believe that non-infectious H. pylori might exist in the oral cavity which is just able to form colonies and invade tissues under special conditions such as concomitant infections (Martinez-Gomis et al, 2006). H. pylori colonization might be necessary for the induction of OLP but not crucially detectable in the generated OLP lesions by PCR or bacterial culture (Riggio et al, 2000;Shimoyama et al, 2000).…”