title: Osteoblasts stimulate osteoclastogenesis via RANKL expression more strongly than periodontal ligament cells do in response to PGE(2).
abstract: OBJECTIVE
  Periodontal ligament cells (PDLs) produce prostaglandin E(2) (PGE(2)) in response to orthodontic force. PGE(2) is a potent osteoclast-inducing factor that induces the receptor activator of nuclear factor-κB ligand (RANKL). Some studies reported that PDLs express RANKL in response to mechanical stress, whereas another study reported that they do not. Based on an immunohistochemical study, RANKL expression is localized around the alveolar bone surface 3 days after tooth movement. However, ankylosed teeth cannot be moved by therapeutic mechanical stress, suggesting that PDLs play a major role in alveolar bone resorption. 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.
  
  
  METHODS
  We examined the expression of RANKL, osteoprotegerin, and macrophage colony-stimulating factor after 48-h culture with or without PGE(2) (10(-11) to 10(-5)M) in HPDLs and HOBs. Then to confirm whether RANKL produced by PGE(2) treatment induces osteoclastogenesis or not, RAW264.7 cells were co-cultured on HPDLs or HOBs pretreated with 10(-6)M of PGE(2).
  
  
  RESULTS
  PGE(2) exposure increased significantly RANKL expression in HOBs compared with HPDLs. PGE(2) exposure significantly decreased osteoprotegerin expression in HPDLs compared with HOBs. 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.
  
  
  CONCLUSIONS
  These results suggest that osteoblasts strongly influence the stimulation of osteoclastogenesis via RANKL, induced by PGE(2) in periodontal tissues, compared with PDLs.
authors.affiliation: Department of Orthodontics, Nihon University School of Dentistry, 1-8-13, Kanda Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan.
authors.forename: Kotoe
authors.initials: K
authors.lastname: Mayahara
authors.forename: Akikuni
authors.initials: A
authors.lastname: Yamaguchi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Takenouchi
authors.forename: Taro
authors.initials: T
authors.lastname: Kariya
authors.forename: Hiroko
authors.initials: H
authors.lastname: Taguchi
authors.forename: Noriyoshi
authors.initials: N
authors.lastname: Shimizu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002478:Cells, Cultured; D018920:Coculture Techniques; D006801:Humans; D007150:Immunohistochemistry; D016173:Macrophage Colony-Stimulating Factor / Q000378:metabolism; D051379:Mice; D010006:Osteoblasts / Q000166:cytology / Q000378:metabolism*; D010010:Osteoclasts / Q000166:cytology / Q000378:metabolism*; D053244:Osteoprotegerin / Q000378:metabolism; D010513:Periodontal Ligament / Q000166:cytology* / Q000378:metabolism*; D011458:Prostaglandins E / Q000494:pharmacology*; D053245:RANK Ligand / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013194:Staining and Labeling; D013314:Stress, Mechanical
chemical_list: D053244:Osteoprotegerin; D011458:Prostaglandins E; D053245:RANK Ligand; D016173:Macrophage Colony-Stimulating Factor