Evidence has continued to support the concept that periodontal infection can serve as a distant site of infection, affecting prematurity and fetal growth.
In women who experience preterm delivery, there is direct biological evidence that periodontal organisms are associated with amniotic fluid inflammation, intrauterine fetal exposure, and fetal inflammation.
Pregnancy is associated with an increase in gingival inflammation and a worsening of periodontal status.
Periodontal diseases, including gingivitis and periodontitis, affect approximately three out of four pregnant women. This increased susceptibility during pregnancy is thought to be attributable to changes in gingival tissue structure, the nature and quality of the host response, and alterations in the oral biofilm composition. Pregnancy provides a special opportunity for the emergence of biofilm pathogens.
Increases in serum progesterone serve to amplify gingival crevicular fluid flow rate, altering conditions within the subgingival flora, and leading to elevated levels of Porphyromonas species. There is an overgrowth of the Socransky Red and Orange complexes. This contributes to an increased prevalence of gingivitis and severity of periodontal disease during pregnancy.
The maternal immune response changes during pregnancy and can be best characterized as a relative state of immunotolerance, which serves to protect the fetus from host versus graft immunorejection.
Thus, alteration in the maternal immune response likely contributes to the increase in gingival inflammation that occurs during pregnancy.
Inflammation can extend beyond the maternal membranes and uterus to promote prematurity, but can also reach the placenta and fetus to impair growth and damage fetal tissues.
Women with preeclampsia were three times more likely to have periodontal infection than healthy normotensive women and that periodontal disease also affects the severity of preeclampsia.