HISTOLOGY AND HISTOPATHOLOGY

From Cell Biology to Tissue Engineering

 

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

Wei Luo1*, Yaqiang Li1*, Zhenhua Luo2 and Baohong Xu1

1Department of Gastroenterology, Beijing Luhe Hospital of Capital Medical University, Beijing and 2Department of Periodontics, Beijing Stomatological Hospital, Capital Medical University, Beijing, PR China
*Contributed equally

Offprint requests to: Baohong Xu, Department of Gastroenterology, Beijing Luhe Hospital of Capital Medical University, No. 82, Xinhua South Road, TongZhou District, Beijing, 101149, P.R. China. e-mail: xbhlwtg@163.com


Summary. 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. Patients 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. Histol Histopathol 35, 665-672 (2020)

Key words: Chronic atrophic gastritis, Periodontitis, cytokines, Helicobacter pylori

DOI: 10.14670/HH-18-187