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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Porphyromonas gingivalis infection at different gestation periods on fetus development and cytokines profile

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Author(s):
Michelin, M. C. A. N. [1] ; Teixeira, S. R. L. ; Ando-Suguimoto, E. S. ; Lucas, S. R. R. [1] ; Mayer, M. P. A. [2]
Total Authors: 5
Affiliation:
[1] Univ Fed Sao Paulo, Dev Biol Lab, Dept Morphol & Genet, Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Microbiol, Lab Oral Microbiol, BR-05508900 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: ORAL DISEASES; v. 18, n. 7, p. 648-654, OCT 2012.
Web of Science Citations: 7
Abstract

Oral Diseases (2012) 18, 648654 Aim: Infective agents may affect pregnancy outcomes by deregulating homeostasis. Objectives: The effects of Porphyromonas gingivalis infection before and at different gestation periods were evaluated. Materials and Methods: Wistar rats infected via subcutaneous with P. gingivalis W83, one week before mating (BM), days 1 (PR1) and 11 of gestation (PR11), and controls were evaluated, and samples were obtained at the end of gestation. P. gingivalis was detected by PCR. Cytokine was determined by ELISA. Results: Infected rats had lower maternal gain of weight. Implantation was not observed in 2/12 BM rats. PR11 presented more fetal-placental resorptions and lower placenta/fetus weight than controls. P. gingivalis was detected in placenta and fetus. IL-6 and TNF-a levels were higher in placenta and serum of infected groups, except for TNF-a in placenta of PR1. IL-1 beta levels were higher in placenta of PR11, but lower in serum and placenta of PR1. There were no differences in IL-10 and PGE2 concentrations among the groups (P < 0.05). Conclusions: The experimental infection by P. gingivalis resulted in alterations in the gestational pattern and in fetal development. The consequences of infection at mid-gestation were more severe than at the beginning, possibly due to the induction of pro-inflammatory cytokines in the fetal compartment. (AU)