Background: Although pregnancy is prone to induce more severe periodontal inflammation and tissue damage, its mechanism remains elusive. Periodontal diseases during pregnancy are associated with adverse pregnancy outcomes including preterm birth or low birth weight. Animal models are ideal for investigating immunological mechanisms in periodontal disease. With a newly modified ligature-induced disease model, we managed to develop periodontal disease in pregnant mice and investigate the immunological mechanism of more severe symptoms during pregnancy. Hypothesis: We hypothesis that P. gingivalis infection during pregnancy will lead to a down-regulation of Treg cells, therefore causing increased inflammation and disease severity. Methods: A ligature-induced murine model for periodontitis has been modified and utilized for periodontal inflammation and tissue damage determination in pregnant mice. Differential expression of inflammatory mediators in mouse gingivae was determined by quantitative real-time PCR. Inflammatory alveolar bone loss was determined by measuring the distance from the cementoenamel junction to the alveolar bone crest (CEJ-ABC). Oral bacteria number was determined by the CFU (Colony Forming Units) count from anaerobic culture of oral swabs. Draining lymph nodes were harvested and analyzed for Treg cells by flow cytometry. Results: In comparison with non-pregnant mice, ligated and P. gingivalis infected pregnant mice displayed significantly (p < 0.05) increased gingival inflammation and periodontal bone loss, accompanied by decreased Treg cells and down-regulated expression of Treg-related molecules and anti-inflammatory cytokines. Conclusion: Our study has established a model to manifest that P. gingivalis infection causes aggravated periodontal disease during pregnancy, possibly through down-regulating Treg numbers and anti-inflammatory capability.
【 预 览 】
附件列表
Files
Size
Format
View
Treg regulation in periodontal disease during pregnancy.