Helicobacter pylori is a microaerophilic organism, which colonizes in the gastric mucosa. Its role in etiology and development of acute and chronic gastritis and peptic ulcer diseases is scientifically proved. Oral cavity especially supragingival, subgingival plaque and so forth simulate the same microaerophilic environment favorable for the growth of this bacterium.Aim:Detection of H. pylori simultaneously in the oral cavity and gastric mucosa of patients suffering from gastric pathologies.Objectives:To detect H. pylori in the oral cavity and gastric mucosa using endoscopy, urease test and real-time polymerase chain reaction (PCR) (urease A gene). Determining its association and corelation with patient demographics, oral hygiene maintenance and periodontal disease status.Materials and Methods:Endoscopic examination, oral findings oral hygiene index-simplified (OHI-S) and community periodontal index and treatment needs (CPITN) indices were recorded. Antral biopsies and supragingival plaque samples were taken from 56 dyspeptic adult patients. The collected samples were subjected to histological examination, urease broth test and urease A gene amplification using real-time PCR.Result:H. pylori was detected in the supragingival plaque of individuals with H. pylori-induced gastric diseases using rapid urease test and real-time PCR analysis. Occurrence of same strain of H. pylori simultaneously in plaque and gastric mucosa was observed. Positive correlation was obtained between the collected indices and quantity of H. pylori colonization.

The inflammatory mediators prostaglandin E2 (PGE2) and interleukin‐1β (IL‐1β) play critical roles in the inflammatory process leading to alveolar bone and connective tissue loss in periodontal disease. Data from a previously published 6‐month clinical study demonstrated that twice daily use of 0.1% ketorolac tromethamine oral rinse prevented alveolar bone loss in adults with periodontitis. We further analyzed data from this study to examine the relationship between PGE2, IL‐1β and bone loss. Patient mean PGE2, and IL‐1β levels in gingival crevicular fluid (M‐GCF) measured throughout the course of the study were directly compared to the maximum amount of alveolar bone height loss observed at a single study site in each patient. The maximum amount of bone loss measured was chosen for the analysis since the pattern of bone loss was clearly episodic in nature. A statistically significant correlation (r = 0.73, p = 0.001) exists between M‐GCF PGE2 concentration and the maximum amount of bone height lost at individual patient study sites. The correlation between M‐GCF IL‐1β concentration and maximum bone height lost is also statistically significant (r = 0.66, p = 0.005). Over the 6‐month duration of the study, both PGE, and IL‐1β were coordinately expressed in the placebo treatment group as reflected in the significant correlation between M‐GCF concentrations of the 2 mediators (r=0.81, p<0.001). Treatment of patients with 0.1% ketorolac tromethamine twice daily for 6 months resulted in reductions of PGE, in GCF and a negligible correlation between M‐GCF PGE, and M‐GCF IL‐1β (r=0.42, p=0.088). This lack of a strong association between the 2 mediators in the ketorolac treatment group provides a direct biochemical readout of the anti‐inflammatory efficacy of ketorolac tromethamine oral rinse in patients with periodontitis. Further studies are warranted to determine the full diagnostic potential of M‐GCF levels of PGE2, and IL‐1β for predicting risk of alveolar bone loss in patients with periodontitis and monitoring periodontal therapy effectiveness.