title: Green tea extract inhibits the   onset of periodontal   destruction in rat   experimental periodontitis.
abstract: OBJECTIVE
  Green tea extract exerts a variety of biological effects, including anti-inflammatory activities. However, there has been no report on the effect of green tea extract on loss of attachment, which is an important characteristic of periodontitis. Here, we examined the inhibitory effects of green tea extract on the onset of periodontitis in a rat model.
  
  
  METHODS
  Rats were immunized intraperitoneally with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 12) received a topical application of LPS onto the palatal gingival sulcus every 24 h. The green tea extract group (n = 12) received a topical application of LPS mixed with green tea extract, sunphenon BG, every 24 h. The phosphate-buffered saline (PBS) group (n = 6) received a topical application of PBS every 24 h. The levels of anti-LPS immunoglobulin G (IgG) in serum were determined using ELISA. Rats in the LPS and green tea extract groups were killed after the 10th and 20th applications. Rats in the PBS group were killed after the 20th application. Loss of attachment, level of alveolar bone and inflammatory cell infiltration were investigated histopathologically and histometrically. RANKL-positive cells and the formation of immune complexes were evaluated immunohistologically.
  
  
  RESULTS
  There was no significant difference in the serum levels of anti-LPS IgG between the LPS group and the green tea extract group. In contrast, loss of attachment, level of alveolar bone, inflammatory cell infiltration and RANKL expression in the green tea extract group were significantly decreased compared with those in the LPS group.
  
  
  CONCLUSIONS
  These findings demonstrate that green tea extract suppresses the onset of loss of attachment and alveolar bone resorption in a rat model of experimental periodontitis.
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshinaga
authors.forename: T
authors.initials: T
authors.lastname: Ukai
authors.forename: S
authors.initials: S
authors.lastname: Nakatsu
authors.forename: A
authors.initials: A
authors.lastname: Kuramoto
authors.forename: F
authors.initials: F
authors.lastname: Nagano
authors.forename: M
authors.initials: M
authors.lastname: Yoshinaga
authors.forename: J L
authors.initials: JL
authors.lastname: Montenegro
authors.forename: C
authors.initials: C
authors.lastname: Shiraishi
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
mesh_terms: D016301:Alveolar Bone Loss / Q000473:pathology / Q000517:prevention & control; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000097:blood; D000936:Antigen-Antibody Complex / Q000032:analysis; D028241:Camellia sinensis; D003238:Connective Tissue / Q000473:pathology; D004195:Disease Models, Animal; D004846:Epithelial Attachment / Q000473:pathology; D004926:Escherichia coli / Q000276:immunology; D007114:Immunization; D007074:Immunoglobulin G / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D010010:Osteoclasts / Q000473:pathology; D017622:Periodontal Attachment Loss / Q000473:pathology / Q000517:prevention & control; D010518:Periodontitis / Q000473:pathology / Q000517:prevention & control*; D010636:Phenols / Q000627:therapeutic use*; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use*; D053245:RANK Ligand / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew
chemical_list: D000893:Anti-Inflammatory Agents; D000907:Antibodies, Bacterial; D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D010636:Phenols; D010936:Plant Extracts; D053245:RANK Ligand; C074269:Sunphenon