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Aggressive and Chronic Periodontitis Correlate With Distinct Cellular Sources of Key Immunoregulatory Cytokines
Author(s) -
Lima Patrícia Maria A.,
Souza Paulo Eduardo A.,
Costa José Eustáquio,
Gomez Ricardo Santiago,
Gollob Kenneth John,
Dutra Walderez Ornelas
Publication year - 2011
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2010.100248
Subject(s) - cd14 , peripheral blood mononuclear cell , tumor necrosis factor alpha , proinflammatory cytokine , immunology , cell adhesion molecule , periodontitis , chronic periodontitis , cd8 , interleukin , integrin alpha m , flow cytometry , cytokine , medicine , inflammation , biology , immune system , in vitro , biochemistry
Background: Chronic periodontitis (CP) and aggressive periodontitis (AP) are inflammatory diseases and the main cause of dental loss in adults. We aimed to investigate the expression of adhesion molecules and the source of proinflammatory and anti‐inflammatory cytokines in circulating mononuclear cells from patients with CP and AP. Methods: Peripheral blood mononuclear cells from healthy controls and CP or AP patients were collected. The expression of the cell adhesion molecules CD11a and CD11b, and the cellular sources of interleukin (IL)‐4, IL‐10, IL‐12, interferon‐γ, and tumor necrosis factor‐α by distinct subpopulations of circulating leukocytes were determined using flow cytometry. Results: The expression of CD11a, but not CD11b, was significantly higher within the CD4 + and CD8 + T cells in CP and AP than in healthy controls. The frequencies of tumor necrosis factor‐α–expressing CD4 + T cells and CD14 + cells were higher in AP and CP, compared to healthy controls, respectively. Moreover, the frequency of IL‐10 expressing CD14 + cells was higher in CP, but not AP, compared to healthy controls CD4 + T cells committed to IL‐4 production was higher in CP than in healthy controls. Conclusion: These results suggest the participation of CD11a in the pathogenesis of periodontal lesions and show distinct cellular sources of immunoregulatory cytokines in AP versus CP.