Shazia A Ansari1, Mehir Un Nisa Iqbal2, Taseer A Khan3, Shahana U Kazmi4. 1. Department of Oral Pathology, Dow Dental College, Dow University of Health Sciences, Karachi, Pakistan. 2. Department of Physiology, University of Karachi, Karachi, Pakistan. Electronic address: mehirunisa@uok.edu.pk. 3. Department of Physiology, University of Karachi, Karachi, Pakistan. 4. Immunology and Infectious Diseases Research Laboratory, Department of Microbiology, University of Karachi, Karachi, Pakistan.
Abstract
AIM: This study was aimed to identify the presence of Helicobacter pylori (H. pylori) genes in oral mucosa and find out their relationship between oral H. pylori infection and gastric complications. METHODS: This study is a case control study consists of 567 subjects with periodontal infection (278 gastric complication cases and 289 controls normal gastric intestinal mucosa) with age range of 20-80 years. Oral health status was recorded by calculating oral hygiene index (OHI), probing depths (PD) and clinical attachment loss (CAL). Each participant provided gastric biopsy and plaque samples which were subjected to H. pylori detection. Polymerase chain reaction (PCR) with different primers specifically β globulin, 16SrRNA, babA, cagA, ureA, ureC and vacA gene was performed which were then analyzed using gel electrophoresis. RESULTS: No significant differences (χ2 = 11.873, p value > 0.05) were observed between oral H. pylori and gastric infections/complications. However, H. pylori increase the risk of developing gastro-esophageal reflux grade II (OR = 1.458, 95%CI = 0.659-3.226), normal upper GIT mucosa with lax esophageal sphincters (OR = 1.215, 95%CI = 0.285-5.181) and duodenal ulcer/duodenitis (OR = 2.187, 95%CI = 0.225-21.278). This study also showed a significant increased risk of gastritis with babA gene. CONCLUSION: Oral pathogenic H. pylori genes may enhance the severity of the gastric infection.
AIM: This study was aimed to identify the presence of Helicobacter pylori (H. pylori) genes in oral mucosa and find out their relationship between oral H. pyloriinfection and gastric complications. METHODS: This study is a case control study consists of 567 subjects with periodontal infection (278 gastric complication cases and 289 controls normal gastric intestinal mucosa) with age range of 20-80 years. Oral health status was recorded by calculating oral hygiene index (OHI), probing depths (PD) and clinical attachment loss (CAL). Each participant provided gastric biopsy and plaque samples which were subjected to H. pylori detection. Polymerase chain reaction (PCR) with different primers specifically β globulin, 16SrRNA, babA, cagA, ureA, ureC and vacA gene was performed which were then analyzed using gel electrophoresis. RESULTS: No significant differences (χ2 = 11.873, p value > 0.05) were observed between oral H. pylori and gastric infections/complications. However, H. pylori increase the risk of developing gastro-esophageal reflux grade II (OR = 1.458, 95%CI = 0.659-3.226), normal upper GIT mucosa with lax esophageal sphincters (OR = 1.215, 95%CI = 0.285-5.181) and duodenal ulcer/duodenitis (OR = 2.187, 95%CI = 0.225-21.278). This study also showed a significant increased risk of gastritis with babA gene. CONCLUSION: Oral pathogenic H. pylori genes may enhance the severity of the gastric infection.