Porphyromonas gingivalis infection induced reproductive abnormalities in mice
10.11855/j.issn.0577-7402.2016.08.08
- Author:
Ke-Min WEI
1
Author Information
1. Department of Stomatology
- Publication Type:Journal Article
- Keywords:
Cytokines;
Infection;
Porphyromonas gingivalis;
Pregnancy;
Premature birth;
Reproductive abnormalities
- From:
Medical Journal of Chinese People's Liberation Army
2016;41(8):653-659
- CountryChina
- Language:Chinese
-
Abstract:
Objective To establish a pregnant mouse model infected with Porphyromonas gingivalis (P.g), and investigate the relationship of P.g infection to prematurity and associated birth abnormalities. Methods Fifty two female mice were randomly divided into P.g infection group (n=26) and control group (n=26). Mice in P.g infection group were anesthetized, the pulp cavity of the first molar was opened and directly injected with W83 strain P.g, and the tooth was then filled. Six weeks after infection, the mice were mated with males and the formation of vagina plug was recorded as 0d. The P.g extracted from the granulation tissue in tooth root was cultivated. The pregnant days and the connatal body weight of infant mouse were recorded, the serum and placental tissue were collected to assess the systemic and local conditions during pregnancy. Results After periodontal P.g infection, the TNF-α, IL-17, IL-6 and IL-1 levels in peripheral blood sera increased significantly. The average gestation was shorter in P.g infection group (18.25d) than in control group (20.45d, P<0.01), and the connatal body weight of infant mouse was also less in the former than in the latter (P<0.01). Immunohistochemistry and PCR revealed the existence of P.g in placenta tissue. P.g infection caused premature rupture of membranes, placental abruption, degeneration and necrosis of trophoblastic and endothelial cells; significantly increased the number of neutrophils and macrophages in placenta tissues, and increased the expression of local TNF-α and COX-2 inflammatory factors at the same time. In P.g infection group, the expressions of CD-31 in endothelial cells of placenta tissues and the apoptotic factor caspase-3 decreased, and the DNA oxidative damage index 8-OHdG increased. Conclusions P.g infection in female mice may cause premature birth and lower connatal body weight of infant mouse, and increase the expression of serous and local inflammatory factors in the placenta. It is suggested that timely removal of periodontitis or gingivitis can prevent some of reproductive abnormalities.
