# New insights into enlarged parietal foramina: an anatomical, radiological, and histological study

## TL;DR

This study investigates enlarged parietal foramina, showing they are likely congenital defects rather than pathological issues, with implications for clinical understanding and treatment.

## Contribution

The study provides the first detailed anatomical, radiological, and histological characterization of enlarged parietal foramina.

## Key findings

- Bilateral EPF were found in 0.8% of examined skulls with smooth, corticated margins.
- Histology showed abrupt cortical thinning and fibrovascular tissue without inflammation or osteoclastic activity.
- EPF are likely congenital defects linked to parietal notch closure and falcine venous structures.

## Abstract

Enlarged parietal foramina (EPF) are rare, symmetric calvarial defects. Although typically benign, they are clinically significant due to possible associations with venous malformations and inherited genetic variants. However, the anatomical, radiological, and histological details of these entities are scant in the medical literature.

Two hundred and fifty adult human skulls from multiple anatomical collections were examined for EPF. Gross morphometric data were supplemented by high-resolution microcomputed tomography (microCT) and histological analysis (H&E, PAS, and Masson’s trichrome). Morphology, cortical continuity, and edge characteristics were evaluated to distinguish developmental defects from acquired bone lesions.

Bilateral EPF were identified in two (0.8%) specimens. MicroCT revealed smooth, corticated margins without lytic or reactive changes. Histological sections demonstrated abrupt cortical thinning and fibrovascular connective tissue at the defect edge, without evidence of osteoclastic activity, inflammation, or abnormal deposition. Surrounding bone exhibited normal cortical and trabecular architecture.

Our findings support the theory that EPF represents a localized congenital ossification defect of the parietal bone rather than a pathologic erosion. Their developmental origin likely reflects aberrant parietal notch closure and persistent falcine venous structures. Understanding their embryologic and genetic basis enhances clinical recognition, guides genetic counseling, and informs surgical management strategies.