Cytokine Production by Oral and Peripheral Blood Neutrophils in Adult Periodontitis
Authors:
- Gillian M. P. GalbraithGGGillian M. P. Galbraith
- Charles HaganCHCharles Hagan
- R. Britt SteedRSR. Britt Steed
- John J. SandersJSJohn J. Sanders
- Tariq JavedTJTariq Javed
- 1 September 1997
- journal article
- research article
- Published by Wiley in Journal of Periodontology
- Vol. 68 (9) , 832-838
Abstract
Proinflammatory cytokines such as tumor necrosis factor‐α (TNF‐α) and interleukin 1β (IL‐1β) also possess bone‐resorptive properties, and are generally considered to play a role in the pathogenesis of periodontal disease. In the present study, TNF‐α and IL‐1β production by oral and peripheral blood polymorphonuclear leukocytes (PMN) was examined in 40 patients with adult periodontitis and 40 orally healthy matched controls. Oral PMN released considerable amounts of both cytokines in unstimulated culture, and. there was no difference between patients and controls when the cytokine levels were corrected for cell number. However, when the effect of disease activity was examined, cytokine release by oral PMN was found to be greatest in patients with advanced periodontitis. Within the healthy control group, IL‐1β production by oral PMN was significantly higher in males (Mann‐Whitney test, P = 0.0008). Examination of IL‐1β production by peripheral blood PMN exposed to recombinant human granulocyte‐macrophage colony stimulating factor revealed no difference between the patient and control groups. In contrast, IL‐1β production by peripheral blood PMN was significantly reduced in patients with advanced disease (Mann‐Whitney test, P = 0.02), and peripheral PMN IL‐1β synthesis was greater in female controls (Mann‐Whitney test, P = 0.054). No effect of race on cytokine production could be discerned in patients or controls. These results indicate that several factors influence cytokine production in oral health and disease, and that a dichotomy in cytokine gene expression exists between oral and peripheral blood PMN in adult periodontitis. J Periodontol 1997;68:832—838.Keywords
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