Title: 0626 - Cyclic Tension Alters Human Dental Follicle Cell Gene Expression in-Vitro
Babak Sarrafpour (Presenter)
The University of Sydney
Philip Boughton, The University of Sydney
Ramin Farahani, The University of Sydney
Stephen Cox, The University of Sydney
Gareth Denyer, The University of Sydney
Elizabeth Kelly, The University of Sydney
Hans Zoellner, The University of Sydney
Objectives: Our earlier finite element analysis suggests jaw strain sensed by dental follicle drives tooth eruption through regulation of bone remodeling. We now explore this possibility studying the response of human dental follicle cells (HDFC) to tension.
Methods: Polycaprolactone scaffolds were seeded with HDFC, and attached to well inserts and magnetic endplates in six well palates. Scaffolds were subjected to cyclic 10% tensile deformation at 1 Hertz for 6, 24 and 48 hours, by uniaxial motion of magnetically-coupled endplates. mRNA was isolated and gene expression compared by cDNA microarray analysis with control cells.
Results: 2319, 3537 and 2268 genes were upregulated at 6, 24 and 48 hrs respectively, while there was downregulation of 2238, 3537 and 3131 genes at these time points. Of these, 669 genes were consistently upregulated, and 662 genes downregulated at all times studied. MetaCore analysis revealed the most regulated gene ontogenies to be for: cytoskeletal remodeling; cell adhesion-chemokines and adhesion; cytoskeleton remodeling-TGF WNT and cytoskeletal remodeling; and cell cycle-ESR1 regulation of G1/S transition. Quantitative RT-PCR confirmed increased MMP10, TIMP1, BMP6 and IL11 involved with bone formation and tissue remodeling.
Conclusions: Results are consistent with our earlier proposed dual role in tooth eruption for dental follicle, as both a mechanosensor for functional jaw strain, and mediator for bone formation beneath roots to raise teeth into the mouth.
This abstract is based on research that was funded entirely or partially by an outside source:
Australian Dental Research Foundation
The submitter must disclose the names of the organizations with which any author have a relationship, the nature of the relationship, and the clinical or research area involved. The following is submitted: None