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Journal of Dental Research
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Clinical

The Involvement of IL-23 and the Th17 Pathway in Periodontitis

H. Ohyama1,*, N. Kato-Kogoe1, A. Kuhara1, F. Nishimura2, K. Nakasho1, K. Yamanegi1, N. Yamada1, M. Hata1, J. Yamane1 and N. Terada1

1 Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan; and
2 Department of Dental Science for Health Promotion, Division of Cervico-Gnathostomatology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan

Correspondence: * ohyama{at}hyo-med.ac.jp

Interleukin (IL)-23 is an essential cytokine involved in expansion of the Th17 lineage, which is associated with many immune-related destructive tissue diseases. We hypothesized that the IL-23-induced Th17 pathway plays a role in periodontal pathology and examined the expression of cytokines, and related molecules, in periodontal lesions and control sites. IL-23 and IL-12 were expressed at significantly higher levels in periodontal lesions than in control sites. However, the relative expression of the IL-23 receptor compared with the IL-12 receptor β2 was significantly higher in periodontal lesions. Moreover, IL-17 expression was significantly higher in periodontal lesions, especially in the tissue adjacent to bone destruction, than in control sites. There was no significant difference in the expression levels of IFN-{gamma}, an important cytokine inhibiting differentiation toward the Th17 pathway, between periodontal lesions and control sites. Together, these results suggest that the IL-23-induced Th17 pathway is stimulated in inflammatory periodontal lesions.

Key Words: periodontitis • interleukin (IL)-23 • Th17 • IL-12 • cellular immune response

This version was published on July 1, 2009

Journal of Dental Research, Vol. 88, No. 7, 633-638 (2009)
DOI: 10.1177/0022034509339889


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