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The role of Hofbauer cells on the pathogenesis of early pregnancy loss

Abstract Introduction Hofbauer cells (HC) are the placental macrophages that play a significant role in many important placental events. The aim of this retrospective study is to investigate the role of HC in the pathogenesis of early pregnancy loss (EPL). Methods The slides were obtained from archi...

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Bibliographic Details
Published in:Placenta (Eastbourne) 2013-12, Vol.34 (12), p.1211-1215
Main Authors: Karakaya, Y.A, Ozer, E
Format: Article
Language:English
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Summary:Abstract Introduction Hofbauer cells (HC) are the placental macrophages that play a significant role in many important placental events. The aim of this retrospective study is to investigate the role of HC in the pathogenesis of early pregnancy loss (EPL). Methods The slides were obtained from archival blocks of missed abortion (MA, n  = 15) and blighted ovum (BO, n  = 15) cases. Unwanted pregnancies materials constituted the control group ( n  = 15). HC and endothelial cells were identified using immunohistochemical methods. HC were counted under light microscope. The extent of villous vasculature was evaluated using two methods; the Chalkey method and microvessel scoring. Results The mean number of villous HC was found to be significantly higher in both MA and BO groups in contrast to the control group. MA group also showed a higher number of HC in comparison with the BO group. Higher microvessel scoring was also found in MA group in contrast to other two groups. Chalkey method revealed no significant difference in the extent of villous vasculature for the control group in comparison with MA and BO. Discussion As we identified relatively low quantity of HC in BO associated with defective vasculature, we hypothesize that an inadequate microvessel formation after hypoxic insult can explain the pathogenesis of BO. We believe that HC are increased in MA due to their divergent roles on immunity and inflammation. Conclusion We therefore conclude that HC may be of biological importance in the pathogenesis of EPL.
ISSN:0143-4004
1532-3102
DOI:10.1016/j.placenta.2013.10.010