Objectives: F-spondin is a secreted neuronal glycoprotein. We first reported F-spondin as a cementoblast specific factor in periodontal tissues. We hypothesized that F-spondin might be involved in cementoclastic differentiation on the root surface. In this study, therefore, we examined the effect of F-spondin on RANKL-mediated cemento/osteoclastogenesis.
Methods: We used RAW246 cells and odontoclast/osteoclast progenitor cells from bone marrow of WT mice. With the chamber assay, we examined the effects of secretary F-spondin from osteoblasts of F-spondin TG mice on RANKL-induced cemento/osteoclast differentiation. Cemento/osteoclastic differentiation was measured by counting tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. The effects of F-spondin on the expression of cemento/osteoclast-related genes were examined by real-time RT-PCR.
Results: Secretary molecules from osteoblasts of F-spondin TG mice significantly inhibited the RANKL-mediated TRAP positive cells from primary progenitor cells with the camber system. Recombinant F-spondin also downregulated RANKL-induced cemento/osteoclast differentiation. F-spondin suppressed TRAP, Cathepsin K, DC-STAMP expressions on the cells. The suppressive effect of F-spondin on RANKL-induced cemento/osteoclast differentiation was partially blocked by knockdown of LDL receptor-related protein 8 (LRP8), a member of the LDL receptor family.
Conclusions: Our findings indicate that F-spondin downregulates differentiation of Cemento/osteoclastic precursors partially via LRP8. It is suggested that F-spondin secreted bycementoblasts may protect the root surface from resorption.