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A 3-D Visualization Technique for Bone Remodeling in a Suture Expansion Mouse Model
Published on: August 18, 2023
Force-induced craniosynostosis in the murine sagittal suture
Adam J Oppenheimer1, Samuel T Rhee, Steven A Goldstein
1Ann Arbor, Mich.; and New York, N.Y. From the Craniofacial Anomalies Program, Section of Plastic Surgery, Department of Surgery, University of Michigan, and the Craniofacial Surgery Program, Department of Surgery, Weill Cornell Medical College.
Cyclical loading of mouse skulls in vitro caused premature suture fusion, mimicking craniosynostosis. This finding suggests abnormal forces contribute to this condition, supporting the role of epigenetic factors.
Area of Science:
- Craniofacial development
- Biomechanical engineering
- Developmental biology
Background:
- Nonsyndromic craniosynostosis etiology is unknown.
- Compressive forces are suspected but not proven to cause premature suture fusion.
- This study investigates force-induced craniosynostosis.
Purpose of the Study:
- To determine if cyclical loading of murine calvaria can induce suture fusion.
- To establish an in vitro model for studying force-induced craniosynostosis.
- To explore the role of mechanical forces in craniosynostosis pathogenesis.
Main Methods:
- Harvested and cultured postnatal day-21 murine calvarial coupons.
- Applied controlled, cyclical, compressive loads (0.3 g for 30 min/day for 14 days) to the sagittal suture in vitro.
- Analyzed suture phenotype using alkaline phosphatase, H&E staining, and bone sialoprotein in situ hybridization.
Main Results:
- Control sutures remained patent, as expected.
- Cyclically loaded sutures exhibited histologic evidence of premature fusion (craniosynostosis).
- Increased alkaline phosphatase activity and bone sialoprotein expression were noted in loaded sutures.
Conclusions:
- Developed an in vitro model for force-induced craniosynostosis.
- Demonstrated that controlled, cyclical, compressive loads can induce premature fusion of the murine sagittal suture.
- Results support the hypothesis that abnormal forces and epigenetic phenomena are crucial in nonsyndromic craniosynostosis pathogenesis.
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