Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • In the present study placental tissue samples obtained only

    2018-10-22

    In the present study, placental tissue samples obtained only from cesarean sections, also the dissection was carried out under sterile condition to reduce the possible vaginal and cervical contamination, even in the control group we tried to select the subject indicated for cesarean section due to prolonged pregnancy, previous cesarean section, suspected placental abruption and fetal distress. In addition, we tried to collect saliva beside GCF samples. Here it should be noted that current option for using saliva as a diagnostic marker has the following advantages: simple, safe and early detection of certain infections [38]. Suggesting that value of using saliva as a diagnostic marker, aided by current technological development will increase rapidly in the near future. Several recent studies have provided provocative evidence for the role of oral infections in the initiation and/or progression of several important systemic conditions [9,39]. Also, the role of bacterial infections in pregnancy complications is well known, it has been shown that intrauterine infections were common among women who gave birth prematurely [40,41]. In this regard, it is worth noting that four possible mechanisms exist for microbes to spread to the uterus, which otherwise a sterile environment: 1) organisms from the vagina and the Eosin Y ascend to the uterus, 2) organisms originate elsewhere in the body and infect placental tissues as a result of hematogenous spread, 3) organisms from the peritoneal cavity translocate retrogradely through the fallopian tube, and 4) organisms are inoculated accidentally in uterine tissues during invasive procedures, such as aminocntesis or chronic villous sampling [42]. Therefore, the possible putative link between chronic oral infection and pregnancy complications might be attributable to repeated exposures of the decidual tissues to periodontal or pericoronal pathogens through transient bacteremia. Previous studies in human showed that oral microorganism, including F.nucleatum and Capnocytophaga sputigena were detected in the amniotic fluid of women with intact membranes and in those with preterm labor [43],[45,46]. Moreover, Madianos and Coworkers have assessed the umbilical cord serum for the presence of fetal immunoglobulin M (IgM) to oral pathogen Porphyromonas gingivalis, documenting a fetal humoral response to organisms distant from the intrauterine environment and suggesting that translocation of oral pathogens to the uteroplacental unit may occur [48]. These studies are supporting again the possibility that oral bacteria or bacterial products can spread through the blood stream to the placenta. A number of experimental studies have linked virulence factors of P. gingivalis to complications in pregnancy outcome. The cysteine proteinases produced by P. gingivalis, termed gingipains are considered to have potentially deleterious effects in activating coagulation factors and platelet aggregation and in altering the cytokine response in human umbilical vein endothelial cells. Fimbriae and Lipopolysaccharide are other important virulence factors of P. gingivalis that can activate peripheral blood monocytes resulting in the release of pro-inflammatory cytokines such as IL-1, IL-6 and TNF-α [49–52]. It is well known that the levels of systemic inflammation are regulated by cytokines such as TNF-α, which act as a key cytokine during inflammatory processes [53]. The results of our study were compatible with the results of many studies that showed that TNF-α contribute to pathologies such as periodontitis and pericoronitis, indicated by the high level of TNF-α in GCF and saliva of both groups [54,55]. We also found higher TNF-α concentration in the serum of patients with preeclampsia when compared to control with statistically significant difference by both ELIZA and PCR techniques. The strong association of TNF-α with preeclampsia is well documented by many studies [53,56]. The increase in TNF-α level simply reflects the natural progression of the inflammatory cascade. Although studies have demonstrated evidence for an inflammatory response both in normal and preeclamptic pregnancies, in preeclampsia inflammation seems excessive [57,58].