Correlation of Aggregatibacter actinomycetemcomitans Detection with Clinical/Immunoinflammatory Profile of Localized Aggressive Periodontitis Using a 16S rRNA Microarray Method: A Cross-Sectional Study

• Published in: PloS one Vol. 8; no. 12; p. e85066
• Main Authors: Gonçalves, Patricia F., Klepac-Ceraj, Vanja, Huang, Hong, Paster, Bruce J., Aukhil, Ikramuddin, Wallet, Shannon M., Shaddox, Luciana M.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 23.12.2013; Public Library of Science (PLoS)
• Subjects: Aggregatibacter actinomycetemcomitans; Aggregatibacter actinomycetemcomitans - genetics; Aggressive Periodontitis - genetics; Analysis; Antibiotics; Bacteria; Blood; Blood cells; Bone loss; Brazil; Chemokines; Clinical trials; Cloning; Cross-Sectional Studies; Cytokines - analysis; Dentistry; Disease; DNA microarrays; E coli; Fibroblasts; Gingival Crevicular Fluid - chemistry; Gum disease; Human subjects; Humans; Inflammation; Inflammatory response; Interleukin 1; Interleukin 8; Lipopolysaccharides; Lipopolysaccharides - blood; Methods; Microarray Analysis - methods; Mitogens; Pathogenesis; Patients; Periodontitis; Peripheral blood; Porphyromonas gingivalis; RNA; RNA, Ribosomal, 16S - genetics; rRNA 16S; Sampling methods; Signal transduction; Tumor necrosis factor-α; Brazil; United States > US; Massachusetts
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0085066

The objective of this study was to determine whether the detection of Aggregatibacter actinomycetemcomitans (Aa) correlates with the clinical and immunoinflammatory profile of Localized Aggressive Periodontitis (LAP), as determined by by 16S rRNA gene-based microarray. Subgingival plaque samples from the deepest diseased site of 30 LAP patients [PD ≥ 5 mm, BoP and bone loss] were analyzed by 16S rRNA gene-based microarrays. Gingival crevicular fluid (GCF) samples were analyzed for 14 cyto/chemokines. Peripheral blood was obtained and stimulated in vitro with P.gingivalis and E.coli to evaluate inflammatory response profiles. Plasma lipopolysaccharide (LPS) levels were also measured. Aa was detected in 56% of LAP patients and was shown to be an indicator for different bacterial community structures (p<0.01). Elevated levels of pro-inflammatory cyto/chemokines were detected in LPS-stimulated blood samples in both Aa-detected and Aa-non-detected groups (p>0.05). Clinical parameters and serum LPS levels were similar between groups. However, Aa-non-detected GCF contained higher concentration of IL-8 than Aa-detected sites (p<0.05). TNFα and IL1β were elevated upon E.coli LPS stimulation of peripheral blood cells derived from patients with Aa-detected sites. Our findings demonstrate that the detection of Aa in LAP affected sites, did not correlate with clinical severity of the disease at the time of sampling in this cross-sectional study, although it did associate with lower local levels of IL-8, a different subgingival bacterial profile and elevated LPS-induced levels of TNFα and IL1β.