INTRODUCTION

Helicobacter pylori is a gram-negative bacillus that colonizes the gastric mucosa and can generate a series of gastric pathologies; dental biofilm is also an area of colonization for said microorganism, which if not taken into account could have a deleterious impact when trying to eradicate said microorganism from the gastric mucosa, since being an extra gastric reservoir could act as a region of potential reinfection^1,2,3,4. Worldwide, helicobacter pylori have been estimated to rise to 4.4 billion infected people⁵, in the continent of South America, a systematic review reported a prevalence of 69.26% (IC95% 64.54-76.99) in adults⁶, at the national level prevalence of 58.7% has been reported in middle and high social strata and> 90% in low social strata⁷. The aforementioned highlights the importance of generating studies to identify factors that predispose to subsequent reinfection to medical treatment, in order to avoid the pathologies and complications of this bacterium.

Helicobacter pylori have virulence factors that influence the magnitude of the damage caused to the gastric mucosa, among which are urease and flagella that guarantee survival and subsequent colonization. Likewise, there are the effector toxins CagA, associated with a more severe inflammatory response and the presentation of MALToma, and vacA, involved in the development of peptic ulcer and gastric cancer.^8-11Infection by this bacterium over the years produces chronic gastritis, which can appear as atrophic, related to the appearance of peptic ulcer due to an imbalance between protective and dec destructive factors¹², and not atrophic, in which there is a loss of the mucous glands^13,14, being replaced by intestinal-type epithelium, called intestinal metaplasia, which can lead to dysplasia of either the gastric epithelium itself or the “intestinalized” one. Finally, if this dysplasia progresses, it will cause an adenocarcinoma.^8,15,17. Another associated entity is MALToma, a mucosa-associated lymphoma, in which H. pylori and specific T cells induce macrophages to produce a cytokine that generates the proliferation of B cells, called APRIL.^11,17

At the global level, there are several studies that have explored the prevalence of helicobacter pylori in dental biofilm in patients with chronic gastritis^{(2,18,19,20,21)}, at the national level in our bibliographic review only 1 was found article in this regard where Chumpitaz et¹⁹found a prevalence of 24.3% being the target population of socioeconomic class between medium and high, without having study subjects of low socioeconomic class, so the present study hopes to find a higher prevalence to that reported.

This article seeks to determine the prevalence of helicobacter pylori in dental biofilm in patients with a diagnosis of chronic gastritis, and exploratory to determine the association between helicobacter pylori in dental biofilm and helicobacter pylori in gastric mucosa biopsy. This is the first work at the national level to mention this association.

METHODS

RESULTS

Of the 100 study subjects evaluated, all presented the necessary data for each of the study variables in this article. The mean and standard deviation of age were 42.01 and 9.24 +/-, the percentage of male and female patients was 52% and 48% respectively, the percentage of helicobacter pylori in dental biofilm was 66% and the percentage of helicobacter pylori in the gastric mucosa was 48% (Table 1). Of the patients positive for helicobacter pylori in gastric mucosa, 83.33% presented positivity in dental biofilm. In an exploratory way, a statistical association was found using the chi-square test for helicobacter pylori in dental biofilm and helicobacter pylori in gastric mucosa with a P-value of 0.002 (Table 2)

DISCUSSION

The present study found a prevalence of 66% of helicobacter pylori in dental biofilm in patients with chronic gastritis, differing from the results presented by Chumpitaz et al, in which prevalence of 24.3 was found % lower than the one we report, which could be explained by the socioeconomic stratum of the population of said study, which is medium-high¹⁹; The article presented is aligned with the prevalence data reported by Asqah et al who reported a prevalence of helicobacter pylori in a dental biofilm of 65% in patients with dyspeptic symptoms in a hospital in Saudi Arabia²and with the work of Desai et al. who found a Helicobacter Pylori prevalence of 98% in a hospital in India²¹; The present study was not aligned with the prevalence results reported by Chitsazi et al, which were 34.1% for patients with pathology diagnosis of chronic gastritis in a hospital in Iran¹⁸, nor with those of Trevizani et al with a prevalence of 39% in a health facility in Brazil²⁰.

There is pathophysiological evidence that takes dental biofilm as a reservoir of helicobacter pylori for future reinfections in patients in patients who have completed antibiotic treatment for gastric infection of helicobacter pylori, dental biofilm is a difficult access environment for antibiotics, which makes The joint work of the dental service is of vital importance since this reservoir could be responsible for harboring Helicobacter strains that may develop antibiotic resistance^2,4,22

Within the limitations of the study, it is worth mentioning that it was unicentric, in only one hospital, the population evaluated exclusively represented the lower middle socioeconomic stratum. This affects the external validity of the work. The present study can be extrapolated to adult populations that are cared for in the hospitals of the Ministry of Health at the level of metropolitan Lima. Studies that analyze the prevalence at the metropolitan lime level in each of the economic strata are recommended since in our bibliographic review no studies were found in this regard, analytical studies are recommended that can analyze the relationship between helicobacter pylori in dental biofilm and helicobacter pylori in gastric mucosa, as well as its association with anthropometric measurements to estimate obesity⁽²³⁾.

CONCLUSION

A high prevalence of helicobacter pylori was found in the dental biofilm of patients with chronic gastritis and an association between dental biofilm and gastric mucosa biopsy for helicobacter pylori, confirming dental biofilm as a reservoir for potential reinfection of the gastric mucosa. Prospective studies are recommended to analyze this association.