• 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
  • Here it is completely clear


    Here, it is completely clear that host tissues in periodontal and pericoronal infections could mount an immune-inflammatory response to bacteria and their byproducts by activating host-derived cytokines such as interleukins 1 and 6 as well as tumor necrosis factor-alpha (TNF-α) and prostaglandin E2 (PGE2) resulting in LY294002 destruction and bone loss [6,12]. It has been proposed that just as periodontal and pericoronal tissue trigger an immune-inflammatory response, there might be a systemic challenge with the resulting inflammatory cytokines including a vascular response in pregnant women, which may relate to various pregnancy complications like preeclampsia, preterm birth and low birth weight [4,12]. In this regard Herrera and coworkers 2001 established that the early identification of risk factors and the treatment of a symptomatic chronic infections lowered the preceding incidences of preeclampsia, they hypothesized that chronic infections may cause increased maternal cytokine levels sufficient to affect vascular endothelial function, thereby making pregnant women prime individuals for the subsequent development of preeclampsia [14].
    Subjects and methods
    Multiplex polymerase chain reaction
    Discussion Chronic oral infections have been implicated as causative agents in a variety of systemic illness including atherosclerotic cardiovascular disease, cerebrovascular ischemia and delivery of a preterm low birth weight infant. Periodontal and pericoronal pathogens were suggested to play a role in systemic diseases either through a direct pro inflammatory effect or through indirect host mediated effects triggered by oral infection [28–30]. Preeclampsia has an ill-defined multifactorial etiology involving both genetic and environmental factors and is associated with an underlying inflammatory dysfunction. Redman and coworkers [11] found that normal pregnancy was characterized by a physiological increase in systemic inflammation and that this response was exaggerated in patients with preeclampsia, they suggested this enhanced response may potentially arise from a decompensating of one or more maternal protective system. The inflammatory response associated with pregnancy and preeclampsia therefore can be assessed systemically by measuring circulatory cytokine profiles [11,13,31]. In this respect, infection of any kind in pregnant women represents a risk for adversities in the developing fetus. Here, it seems logic to hypothesize that chronic oral infection such as periodontitis and pericoronitis associated with increased maternal cytokine levels sufficient to affect vascular endothelial function, may have a significant role in the pathogenesis of preeclampsia, furthermore, in the last decayed several studies have identified the association between chronic oral Gram-negative infection and the development of atherosclerosis and thromboembolic events. In these studies, oral pathogens have been detected in atherosclerotic plaques where it can play a role in the initiation and progression of atherosclerosis leading to coronary vascular disease [28,32,33]. This was explained by the ability of oral Gram-negative pathogens to provide a chronic burden of endotoxins and inflammatory cytokines, which serve to initiate and exacerbate atherogenesis and thrombogenesis [34,35]. Therefore, within the same scenario, it is possible that the placenta may be similarly burdened in pregnant women who develop preeclampsia. In our study, we tried to explore and clarify the evidence of periodontal and pericoronal pathogenic bacteria in human placental tissue for the first time in Egypt to provide further evidence on the association between oral Gram-negative chronic infection and the development of preeclampsia in a sample of pregnant Egyptian women. We have used the RamfJord teeth classification or half mouth examination procedure which is useful in providing maximum clinical information while conserving time and reducing patient and examiner fatigue [36,37].