Trophoblast alterations in the placental bed in relation to physiological changes in spiral arteries

Abstract

Summary. Ninety‐three placental bed biopsies containing a segment of a spiral artery at the level of the decidual–myometrial junction (53 with and 40 without physiological changes) were histologically investigated for depth of trophoblastic penetration of the uterine wall, formation of trophoblastic multinucleated giant cells and the enzyme histochemical characteristics of the interstitial (stromal) and vascular (intramural) trophoblast. The depth of trophoblastic penetration was not related to the presence or absence of the physiological changes. Conversely, in the absence of physiological changes, a significant accumulation of multi‐nucleated giant cells at the decidual–myometrial junction was found before 36 weeks of gestation. The enzyme histochemical characteristics of the placental bed trophoblast suggest a stromal migration of trophoblast to the proximal (decidual–myometrial) part of the spiral artery whereas the distal part might be invaded by intraluminal (upstream) invasion. The hypothesis is put forward that in the absence of physiological changes a disturbed stromal migration is caused by intrinsic (trophoblastic) or extrinsic (interstitial of vascular) factors expressed by the augmentation of the multinucleated cells at the decidual–myometrial junction.

Sensitivity and specificity of finding of multinucleate trophoblastic giant cells in decidua in placentas from high-risk pregnancies

“…Although we are still ignorant about the specific role of mononuclear and multinuclear trophoblasts in the placental bed [18], one of the functions of the extravillous trophoblast (EVT) can be to tolerate hypoxia for successful invasion to occur, whereas other functions may include transformation of the maternal spiral arteries, adherence to and digestion of the extracellular matrix, and interaction with the maternal immune system [19]. Some authors believe that MTGC form because of disturbed migration into the arterial wall, and as a result, prevalence of MTGC is increased in pregnancies in which vascular physiologic changes are lacking [20]. Regulation of human trophoblast migration and invasiveness is complicated and involves many stimulating and inhibiting factors [21,22] that will not be discussed here in detail.…”

“…The findings are in keeping with the observation that, in absence of vascular physiologic changes at the level of decidual-myometrial junction, a significant accumulation of MTGC was found before 36 weeks of gestation. Beyond 36 weeks, whether physiologic changes are present or not, there were only small numbers of MTGC [20]. The increase of extravillous trophoblast in the same conditions as MTGC (Table 1) [31], mutual correlation of those 2 lesions, and similar gestational age profile (Fig.…”

Changes in blood pressure during healthy pregnancy

“…Based on numerous reports describing changes in blood pressure (BP), heart rate (HR), and other hemodynamic variables throughout pregnancy, there has been a general agreement that BP drops in mid-trimester, followed by a progressive increase until term [1][2][3][4][5][6][7][8]. This mid-trimester drop in BP has in part been explained in terms of the development of the low-resistance uteroplacental vascular system [9][10][11] and modification of the renin-angiotensin-aldosterone system [12,13].…”

Estudo da morfologia vascular do leito placentário na hipertensão arterial crônica

“…Foram incluídas gestantes com feto único e vivo, com idade gestacional igual ou superior a 28 semanas e placenta normalmente inserida. Foram excluídas pacientes que apresentaram: descolamento prematuro da placenta, acretismo placentário, malformações fetais, diabete melito, infecções agudas ou crônicas, colagenose, antecedentes de doenças tromboembólicas, tabagismo, pré-eclâmpsia sobreposta, aloimunização pelo fator RH, alcoolismo, nefropatias e fragmentos teciduais do leito placentário que não preencheram os critérios de validação da amostra após avaliação histopatológica 1,18,19 ESTUDO DA MORFOLOGIA VASCULAR DO LEITO PLACENTÁRIO NA HIPERTENSÃO ARTERIAL CRÔNICA Alterações hiperplásicas das camadas íntima e média: definidas pelo espessamento da camada íntima e da camada média (Figura 1d). Necrose caracterizada pela perda celular e eosinofilia intensa de todas as camadas (Figura 1e).…”