Dentistry 3000 (Oct 2017)

Fluctuating dental asymmetry in rabbits with familial nonsyndromic coronal suture synostosis

  • Mae A. Hyre,
  • Seth M. Weinberg,
  • Gregory M. Cooper,
  • James Gilbert,
  • Michael I. Siegel,
  • Mark P. Mooney

DOI
https://doi.org/10.5195/d3000.2017.78
Journal volume & issue
Vol. 5, no. 1
pp. 35 – 44

Abstract

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Fluctuating dental asymmetry has been linked to conditions of unstable pre- and peri-natal development. Familial, nonsyndromic craniosynostosis disrupts early craniofacial development through localized excessive calvarial ossification leading to the premature fusion of the calvarial sutures. Such abnormal gene expression may also produce systemic stress resulting in developmental instability, thereby affecting normal trait symmetry. The present study was designed to test this hypothesis by examining fluctuating dental asymmetry in an inbred strain of rabbits with familial, nonsyndromic coronal craniosynostosis. The mesiodistal (MD) and buccolingual (BL) dimensions of the right and left maxillary first molars were measured in four groups of New Zealand white rabbits (N=176; n=40 with early-onset synostosis, n=65 with delayed-onset synostosis, n=46 in-colony, phenotypically normal rabbits, and n=25 wild-type normal controls). For each variable, raw signed asymmetry was calculated (left-right) and tested for assumptions of fluctuating asymmetry (i.e., normality and non-directionality). Any group that did not meet these assumptions was excluded from further analysis. Using a standard size-adjusted, fluctuating asymmetry index, mean fluctuating asymmetry was calculated and compared across groups with non-parametric statistics. For the MD dimension, no significant (p > 0.05) group differences in mean fluctuating asymmetry were observed among groups. In contrast, rabbits with early-onset synostosis had significantly (p < 0.05) more fluctuating asymmetry in the BL dimension compared to wild-type controls. Results demonstrate increased fluctuating dental asymmetry in rabbits with nonsyndromic, early-onset coronal suture synostosis and suggest that the molecular events producing suture synostosis locally may have also have systemic effects. Knowledge of these systemic interactions may contribute to a fuller understanding of the phenotypic spectrum observed in individuals with nonsyndromic craniosynostosis.

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