Inflammatory lesions in placental pathology

Abstract

Placental inflammatory lesions are important findings that lead fetal and neonatal morbidity and mortality, and can be divided into two broad subcategories, acute inflammation caused by microorganisms and chronic inflammation caused by host immune responses. Recently, a diagnostic framework for these lesions has been established, and uniform diagnostic criteria have been recommended by the Amsterdam International Consensus Group. Chorioamnionitis is representative of the acute inflammatory lesion, and is the most frequent pathological diagnosis in placental pathology. The hallmark of chorioamnionitis is neutrophil infiltration in the membrane/chorioamnionic plate and fetal vessels. The inflammatory response can be both maternal (inflammation in the membrane or chorioamnionic plate) and fetal (inflammation in the fetal vessels-umbilical vessels or chorionic vessel). Recent studies have shown that the fetal inflammatory response is associated with neonatal mortality and morbidity. Furthermore, chronic inflammatory lesions, such as villitis of unknown etiology and chronic histiocytic intervillositis, are also important. Although their etiology remains unknown, the maternal immune response against paternal antigens has been considered a possible factor. These inflammatory lesions are associated with fetal demise and fetal growth restriction. Inflammatory lesions in the placenta are useful for understanding intrauterine conditions, guiding treatment, and predicting complications.

Fetal inflammatory response at the fetomaternal interface: A requirement for labor at term and preterm*

“…The FIR, as mentioned above, is often discussed in association with preterm birth, as it is a major cause of fetal morbidity and mortality 103,153‐155 . However, the current dogma that maternal signals are the sole initiators of human term parturition needs to be reconsidered, and the FIR should be discussed along with maternal inflammatory initiators.…”

“…The FIR, as mentioned above, is often discussed in association with preterm birth, as it is a major cause of fetal morbidity and mortality. 103,[153][154][155] However, the current dogma that maternal signals are the sole initiators of human term parturition needs to be reconsidered, and the FIR should be discussed along with maternal inflammatory initiators. The FIR is not always a response to infectious or etiologic stimuli but may be a natural and physiologic response from the fetus and fetal tissues that maintain and protect pregnancy.…”

“…The FIR is always discussed in the context of infection and preterm birth, 98,102,176 placental pathology, 154 fetal brain injury, 177 and higher neonatal morbidity. 178 The discussion on this topic will resume after discussion of the role of FIR in normal pregnancy and parturition.…”

The Potential Benefit of Hydroxychloroquine in Chronic Placental Inflammation of Unknown Etiology Associated with Adverse Pregnancy Outcomes

“…The histological analyses may reveal areas of inflammatory cells such as lymphocytes, histiocytes, and plasmocytes aggregated within the placenta sometimes with a particular specific location and specific genotypes and phenotypes [ 34 , 35 , 36 ]. Maternal infections such as COVID-19 and cytomegalovirus infection can cause chronic placental inflammation with possible consequences to the fetus; however, unfortunately, a specific etiology is not identifiable in most of the placental inflammation cases [ 34 ].…”

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“…Причиной этого, возможно, является сниженное количество нейротрофических факторов (например, нейротрофического фактора глиальной клеточной линии -glial cell line-derived neurotrophic factor, GDNF) у больных по сравнению с контрольной группой. GDNF участвует в дифференцировке нервной ткани и формировании кишечной нервной системы, поэтому его дефицит может привести к нарушению иннервации и моторики кишки [22][23][24].…”