Journal
BONE
Volume 47, Issue 6, Pages 1020-1029Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2010.08.025
Keywords
Osteopontin; RANKL; PI3K; ERK; Bone remodeling; Mechanical stress
Categories
Funding
- National Institute of Health [R01 DE15425, F-30 FDE 018298A]
- Brodie Endowment
- National Institute of Dental and Craniofacial Research
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Unloading of teeth results in extensive alveolar bone remodeling causing teeth to move in both vertical (super-eruption) and horizontal direction (drift) In order to decipher the molecular mechanisms of unloading-induced bone remodeling during tooth movement we focused on the role of osteopontin (OPN) in the un opposed molar model comparing wild type (WT) and OPN-null mice Our data indicated that OPN was not required for the continuous eruption of un-opposed teeth while OPN was necessary for the drift of teeth OPN expression and osteoclast counts were greatly increased on alveolar bone surfaces facing the direction of the drift in WT mice while osteoclast counts were diminished in OPN-/- mice RANKL expression in the distal periodontal ligament of WT molars increased significantly by day 6 following unloading while overall levels of RANKL expression were decreased in both WT and OPN null mice In vitro treatment of MC3T3 cells WT BMCs and OPN-/- BMCs with recombinant OPN resulted in significantly increased RANKL expression in all three cell types The PI3K and MEK/ERK pathway inhibitors Ly294002 and U0126 reduced RANKL expression levels in vitro Treatment of BMCs and MC3T3 with OPN also resulted in increased ERK phosphorylation and reduced OPG levels Together our studies suggest that increased OPN expression during unloading Induced drifting of teeth enhances localized RANKL expression and osteoclast activity on drift-direction alveolar bone surfaces via extracellular matrix signaling pathways (C) 2010 Elsevier Inc All rights reserved
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