4.4 Article

Levels of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, inflammatory cytokines and species-specific immunoglobulin G in generalized aggressive and chronic periodontitis

Journal

JOURNAL OF PERIODONTAL RESEARCH
Volume 45, Issue 5, Pages 635-642

Publisher

WILEY
DOI: 10.1111/j.1600-0765.2010.01278.x

Keywords

aggressive periodontitis; chronic periodontitis; cytokine; immunoglobulin; bacteria; pathogenesis

Funding

  1. Fond Emile-Beaulieu [93129]
  2. FAPESP(Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [06/60314-5]

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Background and Objective: Aggressive periodontitis pathogenesis still is not completely understood in the literature regarding the relationship between microbial and inflammatory aspects. So this study aimed to compare microbial and inflammatory patterns in the gingival crevicular fluid of generalized aggressive and chronic periodontitis patients. Material and Methods: Forty aggressive and 28 chronic periodontitis patients were selected. Biofilm and gingival crevicular fluid were collected from a deep pocket (periodontal probing depth > 7 mm) and a moderate pocket (periodontal probing depth = 5 mm) of each patient, and microbiological and immunoenzymatic assays were performed. Real-time PCR was used to determine quantities of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Enzyme-linked immunosorbent assay (ELISA) was employed to determine gingival crevicular fluid levels of interleukin-1 beta, interferon-gamma, prostaglandin E-2 and interleukin-10. In addition, immunoglobulin G (IgG) levels against A. actinomycetemcomitans and P. gingivalis lipopolysaccharide were also determined by ELISA. Analysis of variance/Tukey test, Mann-Whitney U-test and the Pearson correlation test were used to determine differences and correlations between variables analysed (alpha = 5%). Results: Patients suffering from generalized aggressive periodontitis had their mouth colonized by higher amounts of A. actinomycetemcomitans and P. gingivalis than chronic periodontitis patients. Conversely, the gingival crevicular fluid levels of IgG against both pathogens were statistically inferior in aggressive periodontitis patients (p < 0.05). With regard to gingival crevicular fluid levels of cytokines, aggressive periodontitis patients presented reduced levels of interleukin-10 (p < 0.05). Conclusion: In comparison to chronic periodontitis, generalized aggressive periodontitis patients have an imbalance in the host response, with reduced levels of interleukin-10 and IgG, and increased periodontal pathogens.

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