title: Human periodontal ligament fibroblast responses to compression in chronic periodontitis.
abstract: OBJECTIVE
  Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis.
  
  
  METHODS
  Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR.
  
  
  RESULTS
  Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs.
  
  
  CONCLUSIONS
  These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.
authors.affiliation: Department of Periodontology, School of Dentistry, Al-Azhar University, Cairo, Egypt.
authors.forename: Ahmed R
authors.initials: AR
authors.lastname: El-Awady
authors.forename: Carol A
authors.initials: CA
authors.lastname: Lapp
authors.forename: Ahmed Y
authors.initials: AY
authors.lastname: Gamal
authors.forename: Mohamed M
authors.initials: MM
authors.lastname: Sharawy
authors.forename: Karl H
authors.initials: KH
authors.lastname: Wenger
authors.forename: Christopher W
authors.initials: CW
authors.lastname: Cutler
authors.forename: Regina L W
authors.initials: RL
authors.lastname: Messer
mesh_terms: D018929:Cell Culture Techniques; D002460:Cell Line; D002478:Cells, Cultured; D018925:Chemokines / Q000032:analysis; D055113:Chronic Periodontitis / Q000473:pathology*; D005347:Fibroblasts / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006874:Hydrostatic Pressure; D018836:Inflammation Mediators / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007378:Interleukins / Q000032:analysis; D020781:Matrix Metalloproteinase 1 / Q000032:analysis; D053513:Matrix Metalloproteinase 16 / Q000032:analysis; D020783:Matrix Metalloproteinase 7 / Q000032:analysis; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D020782:Matrix Metalloproteinases / Q000032:analysis; D010513:Periodontal Ligament / Q000166:cytology* / Q000502:physiology; D013997:Time Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000032:analysis; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000032:analysis
chemical_list: D018925:Chemokines; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D007378:Interleukins; C507102:MMP16 protein, human; C560822:TIMP1 protein, human; C560823:TIMP2 protein, human; D019715:Tissue Inhibitor of Metalloproteinase-1; D019716:Tissue Inhibitor of Metalloproteinase-2; D053513:Matrix Metalloproteinase 16; D020782:Matrix Metalloproteinases; C060932:MMP7 protein, human; D020783:Matrix Metalloproteinase 7; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9; C522360:MMP1 protein, human; D020781:Matrix Metalloproteinase 1