# The Pathophysiology of Wharton’s Jelly and Its Impact on Fetal and Neonatal Outcomes: A Comprehensive Literature Review

**Authors:** Tudor-Andrei Butureanu

PMC · DOI: 10.3390/medsci13040215 · Medical Sciences · 2025-10-02

## TL;DR

Wharton’s jelly protects umbilical vessels, and its abnormalities can lead to serious fetal and neonatal complications like stillbirth and growth restriction.

## Contribution

This paper comprehensively reviews WJ pathophysiology and its direct clinical impact on fetal and neonatal outcomes.

## Key findings

- Reduction or absence of WJ is linked to stillbirth and fetal growth restriction.
- Excessive WJ or edema is associated with maternal diabetes and fetal hydrops.
- Pseudocysts in WJ are markers for chromosomal abnormalities like Trisomy 18 and 13.

## Abstract

Wharton’s jelly (WJ), the mucoid connective tissue of the umbilical cord, provides essential protection to the umbilical vessels against mechanical stress. While research into WJ-derived stem cells for regenerative medicine has surged, the clinical significance of its in utero pathologies remains less explored. This review synthesizes the current literature on the pathophysiology of WJ abnormalities and their direct impact on fetal and neonatal outcomes. Pathologies are broadly categorized as quantitative (absence/reduction or excess/edema) and structural (pseudocysts, mucoid degeneration). A reduction or segmental absence of WJ critically compromises cord integrity, leading to vascular compression and is a direct cause of stillbirth, fetal growth restriction (FGR), and intrapartum distress. Conversely, excessive WJ or edema is associated with maternal diabetes and fetal hydrops and can also impair hemodynamics. Umbilical cord pseudocysts, arising from focal WJ degeneration, are significant markers for severe chromosomal abnormalities, particularly Trisomy 18 and 13, and other structural defects, especially when persistent or multiple. Sonographic measurement of WJ area shows promise as a surrogate for placental function, with decreased area correlating with placental pathology and FGR. However, significant diagnostic challenges persist, particularly the prenatal detection of segmental WJ absence, a “silent” pathology often discovered only after a catastrophic event. This review highlights the critical role of WJ integrity in determining perinatal outcomes and underscores the urgent need for improved diagnostic modalities and standardized management protocols to mitigate associated risks.

## Linked entities

- **Diseases:** stillbirth (MONDO:0041526), fetal growth restriction (MONDO:0005030), fetal hydrops (MONDO:0015193), Trisomy 18 (MONDO:0018071), Trisomy 13 (MONDO:0018068)

## Full-text entities

- **Diseases:** fetal hydrops (MESH:D015160), Trisomy 18 and 13 (MESH:D000073839), stillbirth (MESH:D050497), cord pseudocysts (MESH:D010192), FGR (MESH:D005317), WJ abnormalities (MESH:D000014), edema (MESH:D004487), chromosomal abnormalities (MESH:D002869), WJ absence (MESH:D004832), maternal diabetes (MESH:D003920), WJ degeneration (MESH:D009410)
- **Cell lines:** WJ — Mus musculus (Mouse), Hybridoma (CVCL_U609)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12551069/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12551069/full.md

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Source: https://tomesphere.com/paper/PMC12551069