Abstract
Purpose of Review
There is a growing appreciation within the scientific community that cells exhibit regional variation. Whether the variation is attributable to differences in embryonic origin or anatomical location and mechanical loading has not been elucidated; what is clear, however, is that adult cells carry positional information that ultimately affects their functions. The purpose of this review is to highlight the functions of osteocytes in the craniomaxillofacial (CMF) skeleton as opposed to elsewhere in the body, and in doing so gain mechanistic insights into genetic conditions and chemically-induced diseases that particularly affect this region of our anatomy.
Recent Findings.
In the CMF skeleton, elevated Wnt/β-catenin signaling affects not only bone mass and volume, but also mineralization of the canalicular network and osteocyte lacunae. Aberrant elevation in the Wnt/β-catenin pathway can also produce micropetrosis and osteonecrosis of CMF bone, presumably due to a disruption in the signaling network that connects osteocytes to one another, and to osteoblasts on the bone surface.
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Data Availability
The data presented in this study are available upon request from the corresponding author.
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Acknowledgements
We thank Lauren Menke for her help in revising the manuscript and histological analysis. We thank Jonathan Joseph, Hannah Wagster, and especially McKenna Vicini for their help in histological analysis.
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Contributed to conception and design of the study: P.L. Cuevas, F. Aellos, I.M. Dawid, and J.A. Helms. Contributed to data acquisition, analysis, and interpretation: P.L. Cuevas, F. Aellos, I.M. Dawid, and J.A. Helms. Contributed to drafting and critical revision of the manuscript: P.L. Cuevas, F. Aellos, I.M. Dawid, and J.A. Helms. All authors gave final approval and agreed to be accountable for all aspects of the work.
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Pedro L. Cuevas, Fabiana Aellos and Isaiah M. Dawid shared first authors.
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Cuevas, P.L., Aellos, F., Dawid, I.M. et al. Wnt/β-Catenin Signaling in Craniomaxillofacial Osteocytes. Curr Osteoporos Rep 21, 228–240 (2023). https://doi.org/10.1007/s11914-023-00775-w
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DOI: https://doi.org/10.1007/s11914-023-00775-w