Chronic atrophic gastritis aggravate chronic periodontitis with Helicobacter pylori infection and CD4+Th cytokines infiltration.

OBJECTIVE: To investigate the potential effect of chronic atrophic gastritis on chronic periodontitis and further explore the possible mechanism. METHODS: Local periodontal lesions were collected from periodontitis tissues of 30 CAG patients and 35 control adults without CAG (non-CAG). Clinical periodontal parameters were recorded, and the expression levels of distinct CD4+ Th specific cytokines at local periodontitis lesions were evaluated by real time PCR (RT-PCR). Helicobacter pylori (H. pylori) detection was carried out in both gastric and periodontitis lesions of CAG and non CAG patients. RESULTS: Clinical parameters analysis showed that the level of clinical attachment loss in periodontitis lesions of CAG group was significantly higher than non-CAG group. It was observed that the infection rate of H. pylori in the CAG group was higher than non-CAG group. Further cytokine analysis showed that Th17 associated cytokines IL-17, IL-21 and IL-23 were increased in periodontal lesions of CAG patients when compared with non-CAG patients. However, Th1, Th2, Th9 and Treg cells specific cytokines were not significantly increased in CAG group when compared with non-CAG group. CONCLUSIONS: Datients with CAG demonstrated that significant elevated attachment loss in periodontitis lesions, while elevated Th17 cytokines IL-17, IL-21 and IL-23 participate in immunopathogenesis of both diseases.