Bone fusion in normal and pathological development is constrained by the network architecture of the human skull

TL;DR

This study uses a network model to link skull architecture with the timing of bone fusion, revealing that certain articulations are predisposed to closure in both normal and pathological development, influencing skull morphology.

Contribution

It introduces a network-based approach to quantify skull articulation reliability, connecting topology with craniosynostosis susceptibility and normal developmental timing.

Findings

Articulations with lower reliability scores are linked to craniosynostosis.

Normal skull development involves lower reliability scores at certain articulations.

Skull network topology may epigenetically influence bone fusion timing.

Abstract

The premature fusion of cranial bones, craniosynostosis, affects the correct development of the skull producing morphological malformations in newborns. To assess the susceptibility of each craniofacial articulation to close prematurely, we used a network model of the skull to quantify the link reliability (an index based on stochastic block modeling and Bayesian inference) of each articulation. We show that, of the 93 human skull articulations at birth, the few articulations that are associated with nonsyndromic craniosynostosis conditions have statistically significant lower reliability scores than the others. In a similar way, articulations that close during the normal postnatal development of the skull have also lower reliability scores than those articulations that persist through adult live. These results indicate a relationship between the architecture of the skull network and the specific articulations that close during normal development and in pathological conditions. Our findings suggest that the topological arrangement of skull bones might act as an epigenetic factor, predisposing some articulations to closure, both in normal and pathological development, and also affecting the long-term evolution of the skull.