title: Parathyroid hormone modifies human periodontal ligament cell proliferation and survival in vitro.
abstract: OBJECTIVE
  Periodontal ligament (PDL) cells show traits that are typical of osteoblasts, such as osteoblastic marker gene expression and the ability to respond to parathyroid hormone (PTH) stimulation in an osteoblast-like manner with respect to differentiation and local factor production. In the present study, we hypothesized that human PDL cells might respond to PTH stimulation with changes in proliferation and cell survival and thereby provide another mechanism by which PTH might affect the reparative potential of PDL cells. We speculated that the maturation state of the cells and the mode of PTH(1-34) administration would have an impact on the cellular response.
  
  
  METHODS
  PDL cells were challenged with PTH(1-34) intermittently or continuously at different maturation states. Cell number, 5-bromo-2-deoxyuridine (BrdU) incorporation, DNA fragmentation, nitric oxide production and the duration of the PTH(1-34) effect were determined.
  
  
  RESULTS
  Intermittent PTH(1-34) treatment of preconfluent cells caused a significant increase in proliferation and DNA fragmentation, whereas in more mature cells, proliferation was less enhanced while apoptosis was more pronounced than in immature cells. Continuous PTH(1-34) exposure did not alter proliferation in any maturation state but increased DNA fragmentation in preconfluent cells. PTH(1-34) prevented etoposide-induced apoptosis after 6 h but no longer after 24 h. Nitric oxide production was unaffected.
  
  
  CONCLUSIONS
  These results indicate that human PDL cells respond to PTH(1-34) with changes in proliferative and apoptotic signaling in a maturation-state-dependent manner. Besides changes in local factor production, these findings provide a further possible mechanism to support the idea that PDL cells possess the potential to be involved in the regulation of dental hard tissue repair.
authors.affiliation: Department of Orthodontics, Dental Clinic, University of Bonn, Germany. s.lossdoerfer@gmx.de
authors.forename: S
authors.initials: S
authors.lastname: Lossdörfer
authors.forename: W
authors.initials: W
authors.lastname: Götz
authors.forename: A
authors.initials: A
authors.lastname: Jäger
mesh_terms: D000293:Adolescent; D000818:Animals; D017209:Apoptosis; D002417:Cattle; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002648:Child; D053938:DNA Fragmentation; D006801:Humans; D018377:Neurotransmitter Agents / Q000096:biosynthesis; D009569:Nitric Oxide / Q000096:biosynthesis; D010281:Parathyroid Hormone / Q000378:metabolism* / Q000494:pharmacology*; D010446:Peptide Fragments / Q000378:metabolism* / Q000494:pharmacology*; D010513:Periodontal Ligament / Q000166:cytology / Q000187:drug effects*; D013997:Time Factors
chemical_list: D018377:Neurotransmitter Agents; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D009569:Nitric Oxide