Periodontal diseases (PDs) are common chronic infections affecting tooth-supporting tissues, with an incidence of 46% of the adult population in the United States. [1] It is probably caused by the disequilibrium between infectious pathogens and host-immune response. [2] PDs are considered a potential risk factor for some systemic inflammatory conditions such as cardiovascular diseases, rheumatoid arthritis, diabetes mellitus, and respiratory diseases. [3,4] Moreover, it has been found to be related with adverse pregnancy outcomes, and the main accused mechanism is inflammation for such adverse events. [5] Previous studies have demonstrated that pregnant women with PD have a higher incidence of low-birth weight, preterm birth, and preeclampsia. [6,7] The effect of periodontal inflammation on adverse pregnancy outcomes has been theorized with two different pathways: direct and indirect. First, periodontal bacteria and/or their pathogenic products may directly spread to the fetal-placental unit hematologically or along the genitourinary tract from the oral cavity. Indirectly, local inflammatory mediators such as prostaglandin E2 (PGE2) and tumor necrosis factor-alpha (TNF)-α, which are produced in response to periodontal pathogens may enter the bloodstream, arrive the fetal-placental unit, and amplify the accumulation of this mediators. Similarly, they enter the liver and increase acute-phase protein reaction such as C-reactive protein (CRP) synthesis, and by this way, inflammation in the fetal-placental unit may become more severe. [2] Furthermore, it has been considered that pregnancy could increase the severity of PDs due to hormonal changes.