GINGIVAL CREVICULAR FLUID AND PLACENTAL TISSUE LEVELS OF PENTRAXIN-3 AS A POSSIBLE MARKER FOR PRETERM LABOR IN PATEINTS WITH CHRONIC PERIODONTITIS

Abstract

Pregnancy is normally a healthy physiological procedure that sometimes has opposing outcomes including low birth weight (<2500 grams) and preterm birth (<37 weeks). Preterm birth is now worldwide the second most shared cause of death in children younger than five years after pneumonia. (Sanz M,et al.,2013) As normal pregnancy progresses, amniotic fluid levels of prostaglandin E2 (PGE2) and inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin 1-β (IL-1-β) are raised until a serious threshold is reached to prompt rupture of the amniotic sac membranes, uterine contraction, cervical dilation and delivery. (Haram,et al., 2003) Therefore , normal parturition is controlled by inflammatory signaling and this course represents a triggering mechanism that can be controlled by external stimuli including infection and inflammatory stressors. (Madianos PN,et al.,2013) Adverse pregnancy outcomes (APOs) are usually accompanied with elevated local and systemic inflammatory markers and intrauterine infections. Recent evidence suggests that adverse outcomes are primarily caused by ascending infections from the vagina or cervix or from hematogenous extent from known or unknown non-genital sources. (Sanz M,et al.,2013)

Two major pathways have been recommended to trigger an inflammatory/ immune response and/or suppression of local growth factors in the foetal-placental unit. The direct pathway; where oral microorganisms and/or their components reach foetal-placental unit via hematogenous dissemination from the oral cavity, or oral microorganisms and/or their components reach foetal-placental unit via genitourinary tract. The indirect pathway recommends that inflammatory mediators locally formed in periodontal tissues such as TNF-α and PGE2 circulate and influence the foetal-placental unit, or inflammatory mediators and/or microbial components circulate to the liver, promote cytokine production (e.g. IL-6) and acute phase responses (e.g. C-reactive protein), which then affect the foetal-placental unit. (Sanz M,et al.,2013)