JOURNAL ARTICLE

Aggressive periodontitis and chronic arthritis: blood mononuclear cell gene expression and plasma protein levels of cytokines and cytokine inhibitors

Lars K Sørensen, Anne Havemose-Poulsen, Klaus Bendtzen, Palle Holmstrup
Journal of Periodontology 2009, 80 (2): 282-9
19186969

BACKGROUND: Cytokines and cytokine inhibitors have been associated with many immunoinflammatory diseases. In the present study, we examined whether peripheral blood mononuclear cell (PBMC) gene expression mirrors the corresponding plasma levels of clinically important pro- and anti-inflammatory cytokines and cytokine receptors in patients with periodontitis and patients with arthritis representing two examples of chronic inflammatory diseases, such as periodontitis and arthritis. To identify possible disease-specific characteristics of subjects with periodontitis relative to subjects with chronic inflammation in general, patients with arthritis (juvenile idiopathic arthritis [JIA] and rheumatoid arthritis [RA]) were included.

METHODS: The study population consisted of white adults <35 years of age diagnosed with localized aggressive periodontitis (LAgP; n = 18), generalized aggressive periodontitis (GAgP; n = 27), JIA (n = 10), and RA (n = 23) and healthy controls (n = 25). PBMC transcripts of interleukin (IL) 1 alpha (IL1A), IL 1 beta (IL1B), IL 1 receptor antagonist (IL1RN), IL6, IL10, tumor necrosis factor alpha (TNFA), TNF alpha receptor I (TNFRI), and TNFRII were measured using real-time reverse transcription-polymerase chain reaction and compared to the corresponding plasma protein levels measured by enzyme-linked immunosorbent assay and a multiplex antibody bead assay.

RESULTS: Compared to controls, soluble (s) TNF-RII levels were significantly elevated in patients with GAgP (P = 0.001) or JIA (P = 0.002), and PBMC TNFA transcript levels were lower in patients with JIA (P = 0.001). A negative correlation was found between IL6 expression and IL-6 plasma levels in patients with JIA versus controls, and a positive correlation/association was found between TNFRI expression and sTNF-RI plasma levels in patients with LAgP and RA.

CONCLUSIONS: The study demonstrated only a few changes in the PBMC expression of various cytokine and cytokine inhibitor genes in aggressive periodontitis and chronic arthritis compared to controls. There were a few similarities among disease groups, and no direct and simple correlation between cellular transcripts and proteins was found.

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