Abstract

ABSTRACTThe zygomatic bone is derived evolutionarily from the orbital series. In most modern mammals the zygomatic bone forms a large part of the face and usually serves as a bridge that connects the facial skeleton to the neurocranium. Our aim is to provide information on the contribution of the zygomatic bone to variation in midfacial protrusion using three samples; humans, domesticated dogs, and monkeys. In each case, variation in midface protrusion is a heritable trait produced by one of three classes of transmission: localized dysmorphology associated with single gene dysfunction, selective breeding, or long‐term evolution from a common ancestor. We hypothesize that the shape of the zygomatic bone reflects its role in stabilizing the connection between facial skeleton and neurocranium and consequently, changes in facial protrusion are more strongly reflected by the maxilla and premaxilla. Our geometric morphometric analyses support our hypothesis suggesting that the shape of the zygomatic bone has less to do with facial protrusion. By morphometrically dissecting the zygomatic bone we have determined a degree of modularity among parts of the midfacial skeleton suggesting that these components have the ability to vary independently and thus can evolve differentially. From these purely morphometric data, we propose that the neural crest cells that are fated to contribute to the zygomatic bone experience developmental cues that distinguish them from the maxilla and premaxilla. The spatiotemporal and molecular identity of the cues that impart zygoma progenitors with their identity remains an open question that will require alternative data sets. Anat Rec, 299:1616–1630, 2016. © 2016 The Authors The Anatomical Record Published by Wiley Periodicals, Inc.

Highlights

  • “If these generalizations are meaningful we may suspect that the establishment of the jugal’s squamosal connection, together with the elimination of the constraining connection with the quadratojugal, created a genetic condition in which the jugal had a lot of freedom.”

  • Though much research has focused on cranial vault suture closure in these syndromes, we have shown in humans and mouse models for these conditions that dysmorphogenesis is more severe in the facial skeleton relative to the cranial vault and that distinct facial phenotypes and patterns of variation exist for each diagnostic group (Martınez-Abadıas et al, 2010, 2013a; b; Heuze et al, 2014; Motch Perrine et al, 2014)

  • The principal components analysis (PCA) analysis based on the Procrustes coordinates of the landmarks and semilandmarks that define the global facial configuration reveals three main clusters along PC1, which accounts for 36% of the total shape variation: unaffected individuals, patients diagnosed with Crouzon and Muenke syndrome and patients diagnosed with Apert syndrome (Fig. 5a)

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Summary

Introduction

“If these generalizations are meaningful we may suspect that the establishment of the jugal’s squamosal connection, together with the elimination of the constraining connection with the quadratojugal, created a genetic condition in which the jugal had a lot of freedom.” (http://palaeos.com/vertebrates/bones/dermal/ orbital-jugal2.html). The evolution of higher vertebrates (reptiles, birds, mammals) required changes in developmental patterning that allowed greater variation in jaw morphology affecting individual bones of the facial skeleton. This variation served as the raw material for the evolution of a diverse collection of facial forms of varied widths and degrees of projection and an diverse assortment of zygomatic morphologies. These variants precipitated modifications favored by selection or by genetic drift that became established through changes in development under the control of genes

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