title: Tumor necrosis factor-α and Porphyromonas gingivalis lipopolysaccharides decrease periostin in human periodontal ligament fibroblasts.
abstract: BACKGROUND
  Periostin is a matricellular protein essential for tissue integrity and maturation and is believed to have a key function as a modulator of periodontal ligament (PDL) homeostasis. The aim of this study is to evaluate whether periodontal disease-associated pathogen-related virulence factors (endotoxins/lipopolysaccharides [LPS]) and proinflammatory cytokines alter the expression of periostin in PDL cells.
  
  
  METHODS
  Human PDL cultures were exposed to inflammatory mediators (tumor necrosis factor-α [TNF-α]), bacterial virulence factors (Porphyromonas gingivalis LPS) or a combination in a biomechanically challenged environment. Culture conditions were applied for 24 hours, 4 days, and 7 days. Periostin and TGF-β inducible gene clone H3 (βIGH3) mRNA expression from cell lysates were analyzed. Periostin and βIGH3 proteins were also detected and semiquantified in both cell lysates and cell culture supernatants by Western blot. In addition, periostin localization by immunofluorescence was performed. Analysis of variance and Fisher tests were used to define the statistical differences among groups (P <0.05).
  
  
  RESULTS
  In a mechanically challenged environment, periostin protein was more efficiently incorporated into the matrix compared to the non-loaded controls (higher levels of periostin in the supernatant in the non-loaded group). Interestingly, chronic exposure to proinflammatory cytokines and/or microbial virulence factors significantly decreased periostin protein levels in the loaded cultures. There was greater variability on βIGH3 levels, and no particular pattern was clearly evident.
  
  
  CONCLUSIONS
  Inflammatory mediators (TNF-α) and bacterial virulence factors (P. gingivalis LPS) decrease periostin expression in human PDL fibroblasts. These results support a potential mechanism by which periostin alterations could act as a contributing factor during periodontal disease progression.
authors: Department of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI, USA.
authors: Miguel
authors: M
authors: Padial-Molina
authors: Sarah L
authors: SL
authors: Volk
authors: Juan C
authors: JC
authors: Rodriguez
authors: Julie T
authors: JT
authors: Marchesan
authors: Pablo
authors: P
authors: Galindo-Moreno
authors: Hector F
authors: HF
authors: Rios
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D002478:Cells, Cultured; D005260:Female; D054884:Host-Pathogen Interactions; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D010513:Periodontal Ligament / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D016966:Porphyromonas gingivalis; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; C512835:POSTN protein, human; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha