The elucidation of sharing roles of periodontal ligament cells and alveolar bone osteoblasts in orthodontic-force responsive osteoclast formation.

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Periodontal ligament cells (PDLs) produce PGE_2 during orthodontic tooth movement. PGE_2 is a potent osteoclast-inducing factor that induces RANKL. In this study, we compared the functional difference in osteoclastogenesis between human PDLs (HPDLs) and normal human osteoblasts (HOBs) as a direct effect of PGE_2 exposure.We examined the expression of RANKL with or without PGE_2 in HPDLs and HOBs. Then, RAW264.7 cells were co-cultured on HPDLs or HOBs pretreated with PGE_2. PGE_2 exposure increased significantly RANKL expression in HOBs compared with HPDLs. The number of tartrate-resistant acid phosphatase staining osteoclast-like cells from RAW264.7 cells increased significantly by PGE_2 pretreatment in HOBs and was reduced by small interfering RNA knockdown of RANKL. These results suggest that osteoblasts strongly influence the stimulation of osteoclastogenesis via RANKL, induced byPGE2 in periodontal tissues, compared with PDLs.