title: Topical application of lipopolysaccharide into gingival sulcus promotes periodontal destruction in rats immunized with lipopolysaccharide.
abstract: OBJECTIVE
  The causes of periodontitis are bacteria and the host immune system, but the role of the immune system in the onset and progression of periodontal disease is still unclear. Our previous report showed that the formation of an immune complex in the gingival sulcus induces periodontal destruction. This study was carried out to investigate how the immune system, particularly immunization, is involved in periodontal destruction.
  
  
  METHODS
  Animals immunized intraperitoneally with lipopolysaccharide (LPS) were used as the immunized group. The nonimmunized group received only phosphate-buffered saline. LPS was applied daily onto the palatal gingival sulcus in both groups 1 d after the booster injection. Serum levels of anti-LPS IgG were determined. Loss of attachment and the level of alveolar bone were histopathologically and histometrically investigated. RANKL-bearing cells and the expression of C1qB were immunohistologically evaluated.
  
  
  RESULTS
  The serum levels of anti-LPS IgG were elevated in the early experimental period in the immunized group. There were significant increases in loss of attachment, level of alveolar bone and the number of RANKL-bearing cells in the immunized group. C1qB was observed in the junctional epithelium and adjacent connective tissue. The nonimmunized group showed similar findings at and after the time when the serum level of anti-LPS IgG was elevated.
  
  
  CONCLUSIONS
  Topical application of LPS as an antigen induced periodontal destruction when the serum level of anti-LPS IgG was elevated in rats immunized with LPS. The presence of C1qB suggests that the formation of immune complexes is involved in this destruction.
authors.affiliation: Department of Periodontology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshinaga
authors.forename: T
authors.initials: T
authors.lastname: Ukai
authors.forename: T
authors.initials: T
authors.lastname: Kaneko
authors.forename: S
authors.initials: S
authors.lastname: Nakatsu
authors.forename: C
authors.initials: C
authors.lastname: Shiraishi
authors.forename: A
authors.initials: A
authors.lastname: Kuramoto
authors.forename: K
authors.initials: K
authors.lastname: Oshino
authors.forename: I
authors.initials: I
authors.lastname: Ichimura
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
mesh_terms: D000287:Administration, Topical; D016301:Alveolar Bone Loss / Q000473:pathology; D000818:Animals; D000906:Antibodies / Q000097:blood; D000936:Antigen-Antibody Complex / Q000032:analysis / Q000276:immunology; D015922:Complement C1q / Q000032:analysis; D003238:Connective Tissue / Q000473:pathology; D004846:Epithelial Attachment / Q000473:pathology; D004926:Escherichia coli; D005881:Gingiva / Q000276:immunology* / Q000473:pathology; D007114:Immunization; D007117:Immunization, Secondary; D007074:Immunoglobulin G / Q000097:blood; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides / Q000008:administration & dosage* / Q000276:immunology; D008297:Male; D009504:Neutrophils / Q000276:immunology; D017622:Periodontal Attachment Loss / Q000473:pathology; D010514:Periodontal Pocket / Q000473:pathology; D010518:Periodontitis / Q000276:immunology*; D053245:RANK Ligand / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew
chemical_list: D000906:Antibodies; D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D053245:RANK Ligand; D015922:Complement C1q