The association between periodontitis and some of the problems with pregnancy such as premature delivery, low weight at birth, and preeclampsia (PE) has been suggested. Nevertheless, epidemiological data have shown contradictory data, mainly due to differences in clinical parameters of periodontitis assessment. Furthermore, differences in microbial composition and immune response between aggressive and chronic periodontitis are not addressed by these epidemiological studies. We aimed to review the current data on the association between some of these problems with pregnancy and periodontitis, and the mechanisms underlying this association. Shifts in the microbial composition of the subgingival biofilm may occur during pregnancy, leading to a potentially more hazardous microbial community. Pregnancy is characterized by physiological immune tolerance. However, the infection leads to a shift in maternal immune response to a pathogenic pro-inflammatory response, with production of inflammatory cytokines and toxic products. In women with periodontitis, the infected periodontal tissues may act as reservoirs of bacteria and their products that can disseminate to the fetus-placenta unit. In severe periodontitis patients, the infection agents and their products are able to activate inflammatory signaling pathways locally and in extra-oral sites, including the placenta-fetal unit, which may not only induce preterm labor but also lead to PE and restrict intrauterine growth. Despite these evidences, the effectiveness of periodontal treatment in preventing gestational complications was still not established since it may be influenced by several factors such as severity of disease, composition of microbial community, treatment strategy, and period of treatment throughout pregnancy. This lack of scientific evidence does not exclude the need to control infection and inflammation in periodontitis patients during pregnancy, and treatment protocols should be validated.

Epidemiological data suggest the relationship between periodontitis and preterm deliveries and infants of low weight but little is known about the mechanisms involved in this association. Periodontitis-associated microbiota is quite complex and Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans are considered periodontal pathogens. The potential of P. gingivalis and A. actinomycetemcomitans to induce systemic changes has not yet been fully understood. This study aims to contribute to the understanding of the relationship between infection with periodontal pathogens and adverse effects on pregnancy for determining the effect of experimental infection with P. gingivalis and A.actinomycetemcomitans on pregnancy patterns, level of cytokines and the presence of the pathogen in the foetoplacental unit in mice. The effect of experimental periodontal disease induced by P. gingivalis HW24 D-1 in pregnancy was determined in female mice of the C57BL6 strain. P. gingivalis HW24 D-1 (10 8 CFU) was inoculated by oral gavage for 5 days twice/day in the animal of the test group (n = 9) while the control (n = 5) received only the vehicle in the same manner, volume and periods used for the test group. Twenty-one days after the first oral inoculation, the animals mated and pregnancy was confirmed. On the 16 th day of pregnancy, the animals were sacrificed and the profile of serum cytokines, placental and gingival tissue were determined by ELISA, alveolar bone loss by micro-computed tomography (microCT) and the presence of P. gingivalis by qPCR in samples of oral plaque and gingival tissue, blood, serum, liver, intestine, feces, fetus, placenta and amniotic fluid. Due to lack of an appropriate model of induced periodontitis with A. actinomycetemcomitans in mice, the infection was carried out by intravenous injection with 10 9 CFU of A. Actinomycetemcomitans, JP2 clone in pregnant mice (test, n = 6) on the 3 th , 5 th , 7 th , 11 th and 15 th days of pregnancy, while the control received only the vehicle (n = 5). On the 16 th day of pregnancy, the animals were sacrificed and A. actinomycetemcomitans was detected by qPCR in samples of serum, blood, placenta, fetal and amniotic fluid, the level of cytokines in serum and placental was determined by ELISA. In both models, the effects of the infection on maternal weight gain, weight and number of fetuses and presence of fetal resorption were compared within the test and control animals. In the P. gingivalis model, periodontitis was induced, characterized by alveolar bone loss, since the distance between the cemento-enamel junction to the alveolar bone crest was higher in animals in the test group than the control group (Mann Wittney, p <0,05). The animals of the test group had lower weight at the end of pregnancy, significant difference was observed compared to the control group, there were no statistical difference in the number of fetuses per animal pregnant in both groups, but the weight of the fetuses of the test group were lower compared to fetuses in the control grou...