Salivary and plasma inflammatory mediators and secretory status in preterm delivery women with periodontitis: A cross sectional study

Abstract

Background/Aim. Preterm birth is defined as a delivery prior to the completed 37th week of gestation. Literature data suggested that periodontal processes may influence to the feto-placental unit and induce preterm delivery. The degree of the periodontal disease is influenced by secretor status. Pro-inflammatory cytokines are involved in periodontitis as well as in delivery. The combined influence of these factors on the risk of preterm birth has not been explored. The aim of our study was to investigate the associations between periodontal diseases, secretor status, and interleukin1-b (IL1-ß) and prostaglandine E2 (PGE2) levels in women delivered preterm. Methods. The study included 56 preterm delivery women and 56 women delivered at term as a control group, aged between 17 and 41 years. Periodontal examination, blood and saliva sampling were performed within 48 hours following delivery. Secretor phenotype was determined by hemagglutination inhibition method. The concentrations of IL1-ß and PGE2 were measured by high sensitivity Enzyme-linked Immunosorbent Assay (ELISA). Results. In the pre-term birth group there were 66.1% of women with periodontitis, while in the control one there were 12.5% (p lt 0.01). Concentrations of IL1-ß and PGE2 in plasma were significantly higher in the non-secretor group of women who gave birth pre-term and had periodontitis comparing to other groups. There was a significant correlation between salivary and plasma levels of PGE2 and IL1-ß in the preterm birth group (R = 0.416, p = 0.017 and R = -0.592, p lt 0.001, respectively). There were no such correlations in women who delivered at term. Conclusion. Our results support the hypothesis that non-secretor phenotype and periodontitis are at least in part responsible for pathogenesis of preterm birth. This probability of negative impact of non-secretor status cannot be ignored. These findings support the need for additional research into the biology of human parturition.

Uvod/Cilj. Prevremeni porođaj se definiše kao porođaj pre navršene 37 nedelje gestacije. Podaci iz literature govore u prilog tome da periodontalni procesi mogu uticati na fetoplacentalnu jedinicu i indukovati preterminski porođaj. Sekretorni status može uticati na stepen periodontalne bolesti. Proinflamatorni citokini imaju uticaj na periodontitis kao i na porođaj. Kombinovani uticaj ovih faktora rizika za prevremeni porođaj nije dovoljno istražen. Cilj ove studije je bio da istraži povezanost između periodontalne bolesti, sekretornog statusa, nivoa interleukina 1-b (IL1-b) i prostaglandina E2 (PGE2) kod žena koje su imale prevremeni porođaj. Metode. Studijom je bilo obuhvaćeno 56 žena, koje su imale prevremen porođaj i 56 žena u kontrolnoj grupi koje su se porodile u terminu, starosti između 17 i 41 godine. Periodontalni pregled, uzorkovanje krvi i salive je izvršeno u prvih 48 sati po porođaju. Sekretorni status je određen metodom inhibicije hemaglutinacije. Koncentracije IL1-b i PGE2 su merene visoko senzitivnim Enzyme-linked Immunosorbent Assay (ELISA) testom. Rezultati. U grupi prevremenih porođaja bilo je 66,1% žena sa periodontitisom, a u kontrolnoj grupi 12,5% (p lt 0.01). Prevremeno porođene žena, nesekretori sa periodontitisom imale su u plazmi značajno više vrednosti IL 1-b i PGE 2 u odnosu na ostale grupe (p lt 0,01). U grupi prevremeno porođenih žena postojala je značajna korelacija između salivarnih i plazmatskih koncentracija PGE2 i IL1-b (R = 0.416, p = 0.017 i R = -0,592, p lt 0,001, redom). Ove korelacije nisu postojale kod žena koje su imale terminski porođaj. Zaključak. Naši rezultati podržavaju hipotezu da su sekretorni status i periodontitis, bar delimično, odgovorni za patogenezu preterminskog porođaja. Verovatnoća negativnog uticaja nesekretornog statusa se ne sme ignorisati. Ovi zaključci ukazuju na potrebu za dodatnim istraživanjima porođaja.