Placentation in the Fallopian Tube

Randall, Sarah; Buckley, Hilary; Fox, H.

doi:10.1097/00006254-198801000-00021

Cited by 16 publications

(20 citation statements)

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“…However, the fetomaternal compartment removed from tubal pregnant patients often possesses an integrated fetomaternal interface, as shown in our recent studies (Li et al 2003, Qin et al 2003a. Moreover, tubal pregnancy triggers normal immunoreactivity and hormonal activation of the maternal body (Earl et al 1986, Randall et al 1987, Marx et al 1999, as well as giving rise to immunologically normal and hormonally active trophoblast cells (Vassiliadou & Bulmer 1998, Li et al 2003, Qin et al 2003a. Therefore, tubal pregnancy may provide a unique model to study the mechanism of implantation, particularly from the aspect of trophoblast cells.…”

Section: Introductionmentioning

confidence: 80%

“…Recently, Qin et al (2003a) revealed the switching of ECM and corresponding integrin receptors in trophoblast cells along the invasive pathway in fallopian implantation, and suggested the existence of balanced regulation of trophoblast invasion in tubal pregnancy. Previously, Randall et al (1987) had demonstrated that the early development of the placenta, as well as invasion of the placental bed and tubal vessels by EVCT cells, occurred in the tube in exactly the same way as in the uterine endometrium and spiral arteries. They also suggested that the ability of the blastocyst to implant in the tube, with subsequent normal placentation, might indicate that these processes are purely a function of trophoblastic tissue, with maternal tissues playing only a passive role.…”

Section: Discussionmentioning

confidence: 98%

“…During fallopian implantation, invasion of the maternal blood vessels by EVCT cells also occurs, although the tubal mucosa lacks spiral arteries (Randall et al 1987). Investigations performed in rhesus monkeys showed that during implantation, MMP-2 and -9 are present in EVCT cells within the spiral artery lumen and wall (Blankenship & King 1994, Blankenship & Enders 1997.…”

Section: Discussionmentioning

confidence: 99%

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Dynamic expression of matrix metalloproteinases (MMP-2, -9 and -14) and the tissue inhibitors of MMPs (TIMP-1, -2 and -3) at the implantation site during tubal pregnancy

Bai

Wang²,

Qin³

et al. 2005

Reproduction

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Matrix metalloproteinases (MMPs) are responsible for extracellular matrix (ECM) degradation, and their functions are regulated by tissue inhibitors of MMPs (TIMPs). The evidence for the roles of MMPs and TIMPs in implantation and placentation has remained insufficient in humans, especially during the early stages. Tubal pregnancy has some similarities to normal intrauterine pregnancy and therefore may provide a unique model for implantation studies. In the present study, the expression of MMP-2, -9 and -14, and TIMP-1, -2 and -3 at the feto -maternal interface during tubal pregnancy was examined by immunohistochemistry and in situ hybridization. We found that MMP-9 and TIMP-1, -2 and -3 are produced by all types of extravillous cytotrophoblast (EVCT) cells, while MMP-2 and -14 mainly exist in distal column cytotrophoblast (CCT) cells and invasive EVCT cells. Meanwhile, the intensity of MMP-14 and TIMP-1 and -2 increased along the invasive pathway toward maternal interstitium. In addition, MMP-2, -9 and -14 and TIMP-1, -2 and -3 were all detected in the villous CT (VCT) cells. Furthermore, both the mRNA level and immunoreactivity of MMP-9, TIMP-1 and -3 increased, while those of TIMP-2 decreased concurrent with the progression of pregnancy during weeks 3-9. The unique expression pattern of various MMPs and TIMPs at the feto-maternal interface suggests that they may have roles in regulating the controlled invasion of trophoblasts during implantation and placentation. Meanwhile, the study provides a better understanding of the mechanisms involved in cellular events during human pregnancy, especially at the initiation stage of implantation.

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Section: Introductionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Dynamic expression of matrix metalloproteinases (MMP-2, -9 and -14) and the tissue inhibitors of MMPs (TIMP-1, -2 and -3) at the implantation site during tubal pregnancy

Bai

Wang²,

Qin³

et al. 2005

Reproduction

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“…The mean age of women in group I was 30.16 (22-37) and 29.81 (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36) in group 11. The mean gestational age in group I was 7.69 (s.d.…”

Section: Resultsmentioning

confidence: 99%

“…Failure to express paternal and maternal genome would lead to defective trophoblastic development and embryonic growth failure respectively (25). Randal1 and associates noted that implantation and placentation within the tube are virtually identical to the equivalent process occurring in the uterus (26). Therefore it is reasonable to expect that the ectopic pregnancies with aneuploid DNA content would implant to the tube loosely without showing extensive trophoblastic destruction to the wall.…”

Section: Discussionmentioning

confidence: 99%

DNA ploidy of ectopic pregnancy and first trimester spontaneous abortion investigated by flow cytometry

Erel

Kaleli

Oral

et al. 1996

Acta Obstet Gynecol Scand

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Placenta accreta spectrum: pathophysiology and evidence-based anatomy for prenatal ultrasound imaging

Jauniaux

Collins

Burton

2018

American Journal of Obstetrics and Gynecology

559

542

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Placenta accreta spectrum is a complex obstetric complication associated with high maternal morbidity. It is a relatively new disorder of placentation, and is the consequence of damage to the endometrium-myometrial interface of the uterine wall. When first described 80 years ago, it mainly occurred after manual removal of the placenta, uterine curettage, or endometritis. Superficial damage leads primarily to an abnormally adherent placenta, and is diagnosed as the complete or partial absence of the decidua on histology. Today, the main cause of placenta accreta spectrum is uterine surgery and, in particular, uterine scar secondary to cesarean delivery. In the absence of endometrial reepithelialization of the scar area the trophoblast and villous tissue can invade deeply within the myometrium, including its circulation, and reach the surrounding pelvic organs. The cellular changes in the trophoblast observed in placenta accreta spectrum are probably secondary to the unusual myometrial environment in which it develops, and not a primary defect of trophoblast biology leading to excessive invasion of the myometrium. Placenta accreta spectrum was separated by pathologists into 3 categories: placenta creta when the villi simply adhere to the myometrium, placenta increta when the villi invade the myometrium, and placenta percreta where the villi invade the full thickness of the myometrium. Several prenatal ultrasound signs of placenta accreta spectrum were reported over the last 35 years, principally the disappearance of the normal uteroplacental interface (clear zone), extreme thinning of the underlying myometrium, and vascular changes within the placenta (lacunae) and placental bed (hypervascularity). The pathophysiological basis of these signs is due to permanent damage of the uterine wall as far as the serosa, with placental tissue reaching the deep uterine circulation. Adherent and invasive placentation may coexist in the same placental bed and evolve with advancing gestation. This may explain why no single, or set combination of, ultrasound sign(s) was found to be specific for the depth of abnormal placentation, and accurate for the differential diagnosis between adherent and invasive placentation. Correlation of pathological and clinical findings with prenatal imaging is essential to improve screening, diagnosis, and management of placenta accreta spectrum, and standardized protocols need to be developed.

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Placentation in the Fallopian Tube

Cited by 16 publications

References 0 publications

Dynamic expression of matrix metalloproteinases (MMP-2, -9 and -14) and the tissue inhibitors of MMPs (TIMP-1, -2 and -3) at the implantation site during tubal pregnancy

Dynamic expression of matrix metalloproteinases (MMP-2, -9 and -14) and the tissue inhibitors of MMPs (TIMP-1, -2 and -3) at the implantation site during tubal pregnancy

DNA ploidy of ectopic pregnancy and first trimester spontaneous abortion investigated by flow cytometry

Placenta accreta spectrum: pathophysiology and evidence-based anatomy for prenatal ultrasound imaging

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