CD15 – A new marker of pathological villous immaturity of the term placenta

Seidmann, Larissa; Suhan, Tatyana; Kamyshanskiy, Yevgeniy; Nevmerzhitskaya, A.; Gerein, V.; Kirkpatrick, Charles James

doi:10.1016/j.placenta.2014.07.018

Cited by 28 publications

(16 citation statements)

References 18 publications

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“…The interpretation of the morphology of villous maturation is subjective. Recent studies suggest that the interpretation of maturation disorders might be improved and objectified by immunohistochemistry and molecular analysis .…”

Section: Discussionmentioning

confidence: 99%

Re‐view and view on maturation disorders in the placenta

Turowski

Vogel

2018

APMIS

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Until delivery, the placenta plays an important mediator role between mother and fetus. This unit is affected by peristatic conditions, such as acute or chronic maternal diseases, malnutrition, drugs, and others. But also genetic factors and fetal malformations due to embryonic developmental disorders may contribute to macroscopically visible changes and functional disorders of the placenta. In a constantly ongoing progress of maturation, the placenta records and saves changes due to fetal distress partly as maturation disorders. Understanding of maturation disorders might, therefore, be an important contribution to a better understanding of influences on villous differentiation and might improve follow up and fetal outcome to reduce recurrence risk. However, an internationally unified classification system of maturation disorders does not exist. In this review, terminology, trials, and classifications of villous maturation disorders are summed up and compared, to pinpoint the need of agreement on an international unified and reproducible classification of maturation disorders.

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Section: Discussionmentioning

confidence: 99%

Re‐view and view on maturation disorders in the placenta

Turowski

Vogel

2018

APMIS

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“…[ 10 , 22 – 24 , 26 ] ( Fig 1B ), 3) ‘Thrombosis or intramural fibrin deposition’ was diagnosed as localized, protuberant mural lesions composed of proliferating fibroblasts intermixed with fibrin and erythrocytes in the walls of large placental vessels according to the description of Desa [ 10 , 11 , 22 – 24 , 27 ] ( Fig 1C ), 4) ‘Avascular villi’ was diagnosed as a total loss of villous capillaries and bland hyaline fibrosis in an older lesion. [ 22 , 24 , 28 ] ( Fig 1D ), 5) ‘Delayed villous maturation’ was diagnosed as a monotonous villous population with reduced numbers of vasculosyncytial membranes, increases in the size of distal villi, increased numbers of stromal cells, and interstitial fluid uniformly distributed throughout the villous stroma [ 10 , 11 , 22 – 24 , 29 ] ( Fig 1E ), 6) ‘Maternal inflammatory response’ was diagnosed by the infiltration of neutrophils into the connective tissues of the chorionic plate and/or amnion basement membrane in the fetal surface of the placenta [ 10 , 11 , 22 – 24 , 30 ] ( Fig 1F ), 7) ‘Fetal inflammatory response’ was diagnosed by the infiltration of neutrophils into umbilical vessels or chorionic plate vessels. [ 10 , 11 , 22 , 24 , 26 ] ( Fig 1G ), 8) ‘VUE’ was diagnosed by lymphohistiocytic inflammation predominantly localized to the villous stroma of terminal villi, despite no clinical symptoms of apparent infection in mothers or infants [ 10 , 11 , 22 – 24 , 31 ] ( Fig 1H ), and 9) ‘Deciduitis’ was enrolled as one of the f...…”

Section: Methodsmentioning

confidence: 99%

Placental pathology predicts infantile physical development during first 18 months in Japanese population: Hamamatsu birth cohort for mothers and children (HBC Study)

et al. 2018

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The present study aimed to investigate the relationship between placental pathological findings and physiological development during the neonate and infantile periods. Study participants were 258 infants from singleton pregnancies enrolled in the Hamamatsu Birth Cohort for Mothers and Children (HBC Study) whose placentas were stored in our pathological division. They were followed up from birth to 18 months of age. Physiological development (body weight and the ponderal index [PI]) was assessed at 0, 1, 4, 6, 10, 14, and 18 months. Placental blocks were prepared by random sampling and eleven pathological findings were assessed, as follows: ‘Accelerated villous maturation’, ‘Decidual vasculopathy’, ‘Thrombosis or Intramural fibrin deposition’, ‘Avascular villi’, ‘Delayed villous maturation’, ‘Maternal inflammatory response’, ‘Fetal inflammatory response’, ‘Villitis of unknown etiology (VUE)’, ‘Deciduitis’, ‘Maternal vascular malperfusion’, and ‘Fetal vascular malperfusion’. Mixed model analysis with the use of the xtmixed command by the generic statistical software, Stata version 13.1., identified ‘Accelerated villous maturation’ and ‘Maternal vascular malperfusion’ as significant predictors of a lower body weight and ‘Deciduitis’ as a significant predictor of a small PI, throughout the first 18 months of life. In conclusion, the present study is the first to demonstrate that some pathological findings of the placenta are associated with changes in infantile physical development during the initial 18 months of life in the Japanese population.

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“…“Chorioamnionitis (CAM)” was diagnosed by the infiltration of neutrophils into the connective tissues of the chorionic plate and/or the amnion basement membrane in the fetal surface of the placenta, not in the fetal membrane [ 23 – 25 , 33 ] ( Fig 1D ). “Immature terminal villi” was diagnosed as increases in the size of distal villi, increased numbers of stromal cells, and interstitial fluid uniformly distributed throughout the villous stroma [ 23 – 25 , 34 ] ( Fig 1E ). “Multiple branched terminal villi” was diagnosed as increased numbers of placental villi with the focal formation of tight adherent villous clusters [ 23 – 25 ] typically with syncytial knots [ 35 ] ( Fig 1F ).…”

Section: Methodsmentioning

confidence: 99%

Decrease in Sphingomyelin (d18:1/16:0) in Stem Villi and Phosphatidylcholine (16:0/20:4) in Terminal Villi of Human Term Placentas with Pathohistological Maternal Malperfusion

et al. 2015

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Placental villi play pivotal roles in feto-maternal transportation and phospholipids constitute a major part of the villous membrane. We have been developing and optimizing an imaging system based on a matrix-assisted laser desorption/ionization (MALDI)-based mass spectrometer, which provides clear two-dimensional molecular distribution patterns using highly sensitive mass spectrometry from mixtures of ions generated on tissue surfaces. We recently applied this technology to normal human uncomplicated term placentas and detected the specific distribution of sphingomyelin (SM) (d18:1/16:0) in stem villi and phosphatidylcholine (PC) (16:0/20:4) in terminal villi. In the present study, we applied this technology to nine placentas with maternal or fetal complications, and determined whether a relationship existed between these specific distribution patterns of phospholipid molecules and the six representative pathological findings of placentas, i.e., villitis of unknown etiology (VUE), thrombus, atherosis, chorioamnionitis (CAM), immature terminal villi, and multiple branched terminal villi. In two placentas with the first and second largest total number of positive pathological findings, i.e., five and three positive findings, the specific distribution of SM (d18:1/16:0) in stem villi and PC (16:0/20:4) in terminal villi disappeared. The common pathological findings in these two placentas were atherosis, immature terminal villi, and multiple branched terminal villi, suggesting the possible involvement of the underperfusion of maternal blood into the intervillous space. On the other hand, the number of pathological findings were two or less in the seven other placentas, in which no specific relationships were observed between the differential expression patterns of these two phospholipids in stem and terminal villi and the pathological findings of the placentas; however, the specific distribution pattern of SM (d18:1/16:0) in stem villi disappeared in four placentas, while that of PC (16:0/20:4) in terminal villi was preserved. These results suggested that the absence of the specific distribution of PC (16:0/20:4) in terminal villi, possibly in combination with the absence of SM (d18:1/16:0) in stem villi, was linked to placental morphological changes in response to maternal underperfusion of the placenta.

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CD15 – A new marker of pathological villous immaturity of the term placenta

Cited by 28 publications

References 18 publications

Re‐view and view on maturation disorders in the placenta

Re‐view and view on maturation disorders in the placenta

Placental pathology predicts infantile physical development during first 18 months in Japanese population: Hamamatsu birth cohort for mothers and children (HBC Study)

Decrease in Sphingomyelin (d18:1/16:0) in Stem Villi and Phosphatidylcholine (16:0/20:4) in Terminal Villi of Human Term Placentas with Pathohistological Maternal Malperfusion

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