الفهرس 
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Abstract
Preeclampsia is a syndrome affecting all body systems and is a major cause of maternal and fetal morbidity and mortality worldwide . The pathogenesis of PE is unknown but there are many theories . The most suggestive explanation of PE pathology is the poor placentation.
Telocytes are interstitial cell type that have been identified in many organs either cavitary organs like the Heart (endo , myo and pericardium) , stomach , intestine ,gall bladder ,uterus and fallopian tubes or non-cavitary organs like lungs , pleura and pancreas . TCs have extremely long, thin cytoplasmic extensions that provide a visible direct structural support for surrounding cells. The function of TCs is a subject of research . They were considered as the pacemaker for regulation of contraction of the surrounding smooth muscle fibres .
We postulated that TCs could be linked to poor placental perfusion .In the maternal side , decidual TCs could have a role in abnormal placentation and impaired remodeling of maternal spiral arteries in early pregnancy that leads to PE development in late pregnancy . To prove the hypothesis , our study included examination of the placentae of 20 female patients admitted in the labor ward for caeserian section at Sohag University Hospitals; Obstetrics & Gynecology Department. The cases were selected to be in two groups; 10 cases each; Normal pregnancy (G1) and PE (GII) . Placental and superficial myometrial specimens of the patients were gathered at the time of delivery , processed to develop paraffin sections and stained with Hx & E , TB and Masson trichrom staining . Specimens were also subjected to immunohistochemical study using c-kit monoclonal antibody (CD117) for demonstration of TCs .
Examination of PE group showed cytotrophoblastic cell proliferation and thickened vasculosyncitial membrane . There was a significant increase of the syncytial knot formation associated with apparent increase in villous stromal fibrosis and fibrinoid deposition. These pathological features were considered as one of the causes of impairment of placental barrier function resulting in fetal hypoxia associated with PE.
Thin elongated cells with long and tortious processes were demonstrated by Hx&E and TB stains within the C.T. of the stem, mature intermediate and terminal villi as well as within the decidua and in the superficial myometrium at the site of placentation suggested to be TCs . These cells were confirmed to be TCs using c-kit monoclonal antibody (CD117) as being immunoreactive .The number of villous, decidual and myometrial TCs in GII was significantly reduced in comparison with GI. There was a significant reduction of the number of the migrating EVT cells in the superficial myometrium in GII compared to that in G1.There was a linear correlation between the TCs and EVTCs number in both groups.
Our results clearly demonstrates that villous TCs may play a role in PE associated ischemia and in defective EVT cells migration responsible for remodeling of the spiral arteries result in inadequate blood supply to the fetus and so, development of PE. Further studies are needed to clarify the exact cause of the decreased TCs number weather genetic or developmental during placental formation.