Clinically, severe cemental resorption is a rare consequence of periodontitis, although alveolar bone resorption by osteoclasts is one of the main pathologic changes. F-spondin is a secreted neuronal glycoprotein that localizes to the cementum. F-spondin is among the cementum-specific factors in periodontal tissue that have been reported. However, the effects of F-spondin on osteoclastogenesis have not yet been established. We examined the effects of F-spondin on stages of osteoclastogenesis, migration, and differentiation in a mouse osteoclastic precursor model, RAW 264 cells.Methods:
RAW 264 cells were treated with recombinant F-spondin. Macrophage colony stimulating factor (M-CSF)–induced cell migration was examined by migration assay performed with cell culture inserts. Osteoclastic differentiation was measured by counting tartrate-resistant acid phosphatase (TRAP)–positive multinucleated cells.Results:
In a transmigration assay, F-spondin significantly downregulated M-CSF–induced cell migration. Further, F-spondin significantly reduced the number of receptor activator of nuclear factor-kappa B ligand–induced TRAP-positive multinucleated cells. The receptor-associated protein, an antagonist of the low-density lipoprotein (LDL) receptor family, blocked the effects of F-spondin on M-CSF–induced migration. The suppressive effect of F-spondin on M-CSF–induced cell migration was blocked by knockdown of LDL receptor–related protein 8 (LRP8), a member of the LDL receptor family.Conclusions:
Our findings suggest that F-spondin downregulates recruitment to the root side of periodontal tissue via LRP8 and inhibits differentiation of osteoclastic precursors. It is suggested that F-spondin is essential to protect the root surface from resorption.