Thickening of the amnion basement membrane and its relationship to placental inflammatory lesions and fetal and maternal disorders $ Eumenia C.C. Castro * , Marlene A. Reis, Vicente P.A. Teixeira General Pathology Division, Faculdade de Medicina do Tria ˆngulo Mineiro, Rua Frei Paulino, n30, 38025-180 Uberaba, Minas Gerais, Brazil Received 25 October 2002; received in revised form 2 September 2003; accepted 21 October 2003 Abstract Objective: The aim of this study is the morphological and morphometric analysis of the basement membrane amniotic epithelium of the chorionic plate to establish possible correlation between the basement membrane amniotic epithelium thickening and maternal and fetal disorders. Study design: Ninety-one placentas of infants delivered in Medical Hospital School were studied with hematoxylin-eosin (H&E) and Periodic Acid Schiff (PAS) methods, morphometric and ultrastructural analysis. Results: Of the 91 placentas analyzed, 17 (18.6%) were normal with regard to placental morphology, fetal and maternal history. Basement membrane amniotic epithelium thickening was significantly greater in the cases associated with chorioamnionitis (P ¼ 0:013), villitis (P ¼ 0:040), maternal hypertension syndromes during pregnancy (P ¼ 0:027) and stillborn (P ¼ 0:040) babies. The electron microscopic examination of the basement membrane amniotic epithelium identified a structural alteration and edema of the dense lamina. Conclusion: Thickening of the basement membrane amniotic epithelium was associated with morphologic placental abnormalities and/or fetal or maternal disorders. Thickening of the basement membrane amniotic epithelium was identified away from the site of placental inflammation, possibly being a consequence of cytokines, supporting more than a local effect. This could be a new insight into the pathogenesis of fetal and maternal complications associated with inflammatory placental lesions. # 2003 Elsevier Ireland Ltd. All rights reserved. Keywords: Placenta; Basement membrane; Fetal; Maternal; Disorders; Perinatal 1. Introduction Thickening of the glomerular basement membrane has been correlated with metabolic disease. More recently, thickened basement membrane of the vocal cords has been associated with expected and unexpected infant death and its etiopathogenesis have been studied in many different organs [1–3]. In the placenta, thickening of the basement membrane has most frequently been studied in the trophoblast of the chorionic villi in diabetes [4], smoking [5]; prolonged preg- nancies [6]; hypertension [7–9] and malaria [10]. Thickening of the trophoblast basement membrane has been interpreted as a consequence of hyperplasia of the cytotrophoblast due to hypoxia. In this hypothesis, the cells would increase in number, leading to greater deposition of basement membrane component, thereby provoking thickening [11]. Few studies reporting thickening of the basement mem- brane of the amniotic epithelium in humans were found in the literature. Abnormalities in the amniotic epithelium has been reported in diabetic patients, hydrops fetalis and poly- hydramnios [12–15]. In diabetic rabbits thickening of the basement membranes observed in capillaries of the muscle tissue was considered to be due to a process of replacement of dead cells. The basement membrane of the dead cell would serve as a frame for the cell replacement, without the basement membrane being destroyed afterwards, but rather being retained under the basement membrane of the newly formed cell. In this way, thickening would represent several cell membranes left behind by successive episodes of cell death and replacement [16]. The same authors later demonstrated that cell replace- ment occurs by proliferation or migration of the cells along the pre-existing structure of basement membranes, which may or may not be destroyed afterwards [17]. The prevalence of inflammatory gestational disease is about 40% in some countries and in the second trimester European Journal of Obstetrics & Gynecology and Reproductive Biology 114 (2004) 171–176 $ This study was conducted at the General Pathology Division of School of Medicine of Tria ˆngulo Mineiro, Uberaba, Minas Gerais, Brazil. * Corresponding author. Tel.: þ55-34-3318-5428; fax: þ55-34-33185846. E-mail addresses: eumenia.pat@dcb.fmtm.br (E.C.C. Castro), mareis. pat@dcb.fmtm.br (M.A. Reis), vicpat@dcb.fmtm.br (V.P.A. Teixeira). 0301-2115/$ – see front matter # 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejogrb.2003.10.019