title: Increased bacterial invasion and differential expression of tight-junction proteins, growth factors, and growth factor receptors in periodontal lesions.
abstract: BACKGROUND
  Many pathogens are known to modulate epithelial physical barriers, particularly tight-junction (TJ) proteins, to enter host cells and/or tissues. Growth factors have been implicated in the regulation of TJ proteins. The aim of this study is to determine differences in the levels of TJ proteins, growth factors, and their receptors in relation to bacterial invasion in diseased gingival tissues obtained from patients with periodontitis.
  
  
  METHODS
  The presence of bacteria and expression of junctional adhesion molecule (JAM)-A, occludin, epidermal growth factor (EGF), keratinocyte growth factor (KGF), insulin-like growth factor-I (IGF-I), EGF receptor, KGF receptor, and IGF-1 receptor (IGF-1R) were evaluated in gingival tissues from healthy (n = 10) and diseased (n = 10) sites in patients with periodontitis by in situ hybridization and immunohistochemistry.
  
  
  RESULTS
  The bacterial invasion of gingival tissue was increased in periodontal lesions compared with healthy sites. Although the levels of JAM-A and occludin were not significantly different between the healthy and diseased sites, aberrant cytoplasmic expression of JAM-A and occluding was often observed in the lesions. In addition, more leukocytes expressing JAM-A or occludin were observed within the disease-associated epithelia. Compared with the healthy sites, the differential expression of KGF, IGF-I, and IGF-1R was observed in the periodontal lesions. The levels of TJ proteins showed positive correlations with those of growth factors.
  
  
  CONCLUSIONS
  The aberrant expression of growth factors and TJ proteins may contribute to increased bacterial invasion and disease progression in periodontal lesions.
authors: Department of Immunology and Molecular Microbiology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Korea.
authors: Yun S
authors: YS
authors: Choi
authors: Yong C
authors: YC
authors: Kim
authors: Suk
authors: S
authors: Ji
authors: Youngnim
authors: Y
authors: Choi
mesh_terms: D000328:Adult; D001419:Bacteria / Q000472:pathogenicity*; D058491:Bacterial Load; D015815:Cell Adhesion Molecules / Q000032:analysis; D003593:Cytoplasm / Q000737:chemistry; D018450:Disease Progression; D004815:Epidermal Growth Factor / Q000032:analysis; D004846:Epithelial Attachment / Q000737:chemistry / Q000382:microbiology; D066246:ErbB Receptors / Q000032:analysis; D005260:Female; D051523:Fibroblast Growth Factor 7 / Q000032:analysis; D005881:Gingiva / Q000737:chemistry* / Q000382:microbiology; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis*; D007962:Leukocytes / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D062793:Occludin / Q000032:analysis; D010518:Periodontitis / Q000378:metabolism* / Q000382:microbiology; D017526:Receptor, IGF Type 1 / Q000032:analysis; D011956:Receptors, Cell Surface / Q000032:analysis; D017978:Receptors, Growth Factor / Q000032:analysis*; D062725:Tight Junction Proteins / Q000032:analysis*
chemical_list: D015815:Cell Adhesion Molecules; C407243:F11R protein, human; C496453:FGF7 protein, human; D036341:Intercellular Signaling Peptides and Proteins; C568985:OCLN protein, human; D062793:Occludin; D011956:Receptors, Cell Surface; D017978:Receptors, Growth Factor; D062725:Tight Junction Proteins; D051523:Fibroblast Growth Factor 7; D004815:Epidermal Growth Factor; D007334:Insulin-Like Growth Factor I; D066246:ErbB Receptors; D017526:Receptor, IGF Type 1
keywords: Epidermal growth factor; fibroblast growth factor 7; immunohistochemistry; insulin-like growth factor I; periodontitis; tight junction proteins