Literature DB >> 16922931

Immunoglobulin G subclass antibody profiles in Porphyromonas gingivalis-associated aggressive and chronic periodontitis patients.

Y Takeuchi1, M Aramaki, T Nagasawa, M Umeda, S Oda, I Ishikawa.   

Abstract

BACKGROUND/AIMS: The immunoglobulin G (IgG) antibody response is considered to be protective and beneficial for the control of periodontal lesions. This study analysed IgG subclass antibody levels of Porphyromonas gingivalis in patients with both aggressive periodontitis (AgP) and chronic periodontitis (CP).
METHODS: Subgingival plaque and peripheral blood samples were collected from patients with localized AgP (n = 13), generalized AgP (n = 28) and generalized CP (n = 27) and from 14 periodontally healthy controls. P. gingivalis was identified in subgingival pockets using a polymerase chain reaction. Simultaneously, serum IgG subclass antibody against P. gingivalis whole cells/P. gingivalis fimbriae were measured using enzyme-linked immunosorbent assay.
RESULTS: P. gingivalis was frequently detected in periodontitis patients. Anti-P. gingivalis whole cell IgG1 was elevated in all P. gingivalis-positive patients in the three periodontitis groups. Although increased anti-P. gingivalis IgG1 was also observed in the bacterium-positive healthy controls, the level was lower than that found in the three periodontitis groups. Levels of IgG1, IgG2, IgG3 and IgG4 to P. gingivalis did not differ among bacterium-positive patients in the three periodontitis groups; a significant increase of IgG2 level was not observed in localized AgP. Anti-fimbriae IgG subclass levels of IgG1, IgG2 and IgG4 did not differ among bacterium-positive subjects in all groups, while the anti-fimbriae IgG3 level in generalized CP was significantly higher than that in localized and generalized AgP.
CONCLUSIONS: P. gingivalis infection elicited an IgG subclass antibody response in both periodontitis patients and healthy subjects, while higher anti-P. gingivalis IgG1 levels were found in the three periodontitis groups compared with the healthy control group.

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Year:  2006        PMID: 16922931     DOI: 10.1111/j.1399-302X.2006.00296.x

Source DB:  PubMed          Journal:  Oral Microbiol Immunol        ISSN: 0902-0055


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