title: Human periodontal ligament cells express osteoblastic phenotypes under intermittent force loading in vitro.
abstract: Mechanical strain applied to bone leads to bone remodeling. In the oral cavity, it is unclear how such mechanical force applied to move teeth orthodontically induces alveolar bone remodeling. It is known that osteoclasts are the only cells that are responsible for bone resorption, while the formation and activity of osteoclasts are regulated by osteoblasts. So it is believed that osteoblasts play an important role not only in bone formation but in bone remodeling as well. Therefore, the purpose of this study was to examine the effect of mechanical force on human periodontal ligament (PDL) cells and whether they express osteoblastic characters in vitro.
  
  
  METHODS
  Human PDL cells cultured in vitro were loaded with intermittently stretching force for 24 hours. The expression of alkaline phosphatase (ALP), osteocalcin (OCN) and osteoprotegerin (OPG) were detected at mRNA and protein levels at 0, 2nd, 4th, 6th, 12th, 24th hours after intermittent force loading.
  
  
  RESULTS
  Without any stimulation, ALP and OPG mRNA expressions were detected in human PDL cells by in-situ hybridization, but not that of OCN mRNA. ALP mRNA signal was up-regulated and that of OPG was down-regulated by mechanical force within 24 hours. OCN mRNA expression was induced by mechanical force in the late phase of the 24-hours loading cycle. The changes in secreted proteins showed similar results with those seen at the mRNA level.
  
  
  CONCLUSIONS
  Human PDL cells express osteoblastic phenotypes under intermittent force loading and play a role in alveolar bone remodeling.
authors.affiliation: Department of Orthodontics, Peking University School of Stomatology, Beijing, China.
authors.forename: Y Q
authors.initials: YQ
authors.lastname: Yang
authors.forename: X T
authors.initials: XT
authors.lastname: Li
authors.forename: A B M
authors.initials: AB
authors.lastname: Rabie
authors.forename: M K
authors.initials: MK
authors.lastname: Fu
authors.forename: D
authors.initials: D
authors.lastname: Zhang
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D016723:Bone Remodeling; D002478:Cells, Cultured; D015536:Down-Regulation; D005347:Fibroblasts / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D017403:In Situ Hybridization; D066298:In Vitro Techniques; D015233:Models, Statistical; D010006:Osteoblasts / Q000166:cytology / Q000378:metabolism*; D015675:Osteocalcin / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism; D053244:Osteoprotegerin; D010513:Periodontal Ligament / Q000166:cytology*; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D013314:Stress, Mechanical; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D006023:Glycoproteins; D053244:Osteoprotegerin; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human; D015675:Osteocalcin; D000469:Alkaline Phosphatase