Helicobacter Pylori in periodontal pockets of chronic periodontitis patients with and without type II diabetes mellitus: a randomized controlled trial

Abstract

This randomized controlled study evaluated the association of Helicobacter pylori (H. pylori) with chronic periodontitis patients with and without type II Diabetes Mellitus. H. pylori is considered to be a pathogen responsible for gastritis, peptic ulcers and a risk factor for gastric cancer. The aim of the present study was to evaluate the association of H. pylori with chronic periodontitis patients with and without type II diabetes mellitus before and after treatment. The prevalence of H. pylori in periodontal pockets was determined by rapid urease test in a 36 patients, which were grouped as Group 1 (Healthy subjects), Group II (chronic periodontitis patients) and Group III (Chronic periodontitis patients with Type II Diabetes Mellitus), 12 in each group before treatment by collecting plaque samples. After treatment, 12 plaque samples were collected and prevalence H. pylori was detected. Group II and Group III had a significantly higher rate of positive results for H. pylori compared to healthy subjects before treatment. After treatment, H. pylori were not detected in Group II and in Group III Only one of 12 chronic periodontitis patients with Type II diabetes mellitus had H. pylori in the periodontal pocket. The prevalence of H. pylori did not differ significantly between the chronic periodontitis patients with and without type II diabetes mellitus. Meticulous scaling and root planning will reduce the prevalence of H. pylori in periodontal pockets.

Genotyping of the Helicobacter pylori isolates of raw milk and traditional dairy products

“…1 Though Helicobacter pylori (H. pylori) have been considered as a main cause of mucosa associated lymphoma, peptic ulcer disease, type B gastritis, and gastric adenocarcinoma, roles of foods and especially dairy products in its transmission are still unknown. [2][3][4] H. pylori was found in stomach of domestic animals in the absence of associated gastritis, it was recovery from milk, meat and gastric tissue of domestic ruminants suggest that domestic animals and their milk may be reservoirs of H. pylori. [2][3][4] Suitable circumstances for growth and survival of H. pylori in milk and dairy products provide adequate settings for transmission of H. pylori from these foodstuffs to human.…”

“…[2][3][4] H. pylori was found in stomach of domestic animals in the absence of associated gastritis, it was recovery from milk, meat and gastric tissue of domestic ruminants suggest that domestic animals and their milk may be reservoirs of H. pylori. [2][3][4] Suitable circumstances for growth and survival of H. pylori in milk and dairy products provide adequate settings for transmission of H. pylori from these foodstuffs to human. 5 The severity of clinical complications caused by H. pylori is depends on several factors.…”

The Association between Oral Hygiene and Gastric Pathology in Patients with Dyspepsia: a Cross-Sectional Study in Southeast Iran

“…24 In contrast, Berroteranand co-workers found no relationship between HP infection and periodontal disease (Loe and Sillness indices), dental caries, and dental hygiene. 25 In this research,it was specified that periodontal diseases and DMFT indexhad meaningful relationship with gastric HP infection.Some studies have declared that shift in oral flora and systemic inflammation can affect some organs such as stomach, and pancreas 28 and result in tumor development and growth. 16 …”

The Benefits of Non-Surgical Periodontal Treatment in Association with Gastric Eradication

“…Over the years several researchers have pondered on and studied the association between periodontal disease and Hp infection. They obtained positive results on the presence of the bacterium in the oral cavity and above all on the association of the two diseases suggesting that the oral cavity acts as an extra-gastric reservoir [10]. Furthermore, Gürbüz et al [7] reported a positive association between levels of dental plaque and the levels of gastric and oral Hp.…”