This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Beklen, A. Articles by Konttinen, Y.T. Search for Related Content PubMed PubMed Citation Articles by Beklen, A. Articles by Konttinen, Y.T. Social Bookmarking                   What's this?

MMPs, IL-1, and TNF are Regulated by IL-17 in Periodontitis

¹ Department of Medicine/Invärtes medicin, Helsinki University Central Hospital, Helsinki, Finland;
² Institute of Biomedicine/Anatomy, University of Helsinki, Finland;
³ Medico-social Centre, Dental Clinic, Bogazici University, Istanbul, Turkey;
⁴ ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland;
⁵ Department of Periodontology, Faculty of Dentistry, Ankara University, Turkey;
⁶ Institute of Dentistry, University of Helsinki, Dept. of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Finland;
⁷ COXA Hospital for Joint Replacement, Tampere, Finland

Correspondence: ^* corresponding author, yrjo.konttinen{at}helsinki.fi, Biomedicum Helsinki, PO Box 700 (Haartmaninkatu 8), FI-00029 HUS-Finland

Periodontitis is characterized by periodontal tissue destruction. Since interleukin-17 (IL-17) has been reported to up-regulate IL-1β and tumor necrosis factor-alpha (TNF-), it was hypothesized that it is increased in periodontitis and up-regulates these cytokines and tissue-destructive matrix metalloproteinases (MMP) in local migrant and resident cells. Immunocytochemistry disclosed elevated IL-1β, TNF-, and IL-17 levels in periodontitis. These cytokines induced proMMP-1 and especially MMP-3 in gingival fibroblasts, whereas MMP-8 and MMP-9 were not induced. IL-17 was less potent as a direct MMP inducer than IL-1β and TNF-, but it induced IL-1β and TNF- production from macrophages, and IL-6 and IL-8 from gingival fibroblasts. In accordance with these findings, immunocytochemistry disclosed that MMP-1 and MMP-3 were increased in periodontitis. Gingival fibroblasts may play an important role in tissue destruction in periodontitis via cytokine-inducible MMP-1 and MMP-3 production, in which IL-17 plays a role as a key regulatory cytokine.

Key Words: IL-1β • TNF- • IL-17 • MMP • periodontitis

Journal of Dental Research, Vol. 86, No. 4, 347-351 (2007)
DOI: 10.1177/154405910708600409


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				M. Hashizume, N. Hayakawa, and M. Mihara IL-6 trans-signalling directly induces RANKL on fibroblast-like synovial cells and is involved in RANKL induction by TNF-{alpha} and IL-17 Rheumatology, November 1, 2008; 47(11): 1635 - 1640. [Abstract] [Full Text] [PDF]

				D. M. Cortez, M. D. Feldman, S. Mummidi, A. J. Valente, B. Steffensen, M. Vincenti, J. L. Barnes, and B. Chandrasekar IL-17 stimulates MMP-1 expression in primary human cardiac fibroblasts via p38 MAPK- and ERK1/2-dependent C/EBP- , NF-{kappa}B, and AP-1 activation Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3356 - H3365. [Abstract] [Full Text] [PDF]