title: The formation of immune complexes is involved in the acute phase of periodontal destruction in rats.
abstract: OBJECTIVE
  Loss of clinical attachment and alveolar bone destruction are major symptoms of periodontitis, caused by not only the destructive effect of periodontopathic bacteria but also the overactive response of the host immune system against periodontal pathogens. The details of the participation of the immune system in the onset and progression of periodontitis are unclear. In this study, we attempted to determine whether the host immune system, and in particular the formation of immune complexes, is involved in the periodontal destruction.
  
  
  METHODS
  We applied ovalbumin or lipopolysaccharide (LPS) as antigens and their specific immunoglobulin G (IgG) antibodies purified from rat serum to rat gingival sulcus alternately. Loss of attachment, alveolar bone destruction and the numbers of inflammatory cells infiltrating the periodontal tissue and osteoclasts on the alveolar bone surface were investigated histometrically. The formation of immune complex was confirmed by immunohistological staining of complement C1qB.
  
  
  RESULTS
  Loss of attachment and the presence of C1qB were observed histopathologically in both experimental groups. The group that had been treated with LPS and anti-LPS IgG showed greater loss of attachment. The number of inflammatory cells in the periodontal tissue was increased in both experimental groups, while osteoclasts at the alveolar bone crest were observed only in the group that had been treated with LPS and anti-LPS IgG.
  
  
  CONCLUSIONS
  In the present study, we showed that the formation of immune complex appears to be involved in the acute phase of periodontal destruction and that the biological activity of antigens is also important.
authors.affiliation: Department of Periodontology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Kuramoto
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshinaga
authors.forename: T
authors.initials: T
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Ukai
authors.forename: C
authors.initials: C
authors.lastname: Shiraishi
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: D016301:Alveolar Bone Loss / Q000097:blood / Q000276:immunology* / Q000382:microbiology*; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D000936:Antigen-Antibody Complex; D000942:Antigens, Bacterial / Q000097:blood / Q000276:immunology; D018960:Hyaluronan Receptors / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D024101:Mitochondrial Proteins; D010010:Osteoclasts / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D017622:Periodontal Attachment Loss / Q000097:blood / Q000276:immunology* / Q000382:microbiology*; D051381:Rats; D011917:Rats, Inbred Lew
chemical_list: D000907:Antibodies, Bacterial; D000936:Antigen-Antibody Complex; D000942:Antigens, Bacterial; C490195:C1qbp protein, rat; D018960:Hyaluronan Receptors; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D024101:Mitochondrial Proteins; D010047:Ovalbumin