Journal of Dental Research, Vol 76, 1833-1839, Copyright © 1997 by International & American Associations for Dental Research Online Journals

ARTICLES

Profile of cytokine mRNA expression in chronic adult periodontitis

F. A. Roberts, K. A. McCaffery and S. M. Michalek
Department of Periodontics, School of Dentistry, The University of Alabama at Birmingham, 35294-2170, USA.

Chronic inflammation induced by bacteria often leads to host-mediated destruction of tissues adjacent to the sites of microbial insult. The chronic inflammatory process of adult periodontitis results in the destruction of supporting osseous and connective tissues of the teeth. We hypothesized that virulence factors of periodontal pathogens such as lipopolysaccharide stimulate inflammatory cytokine expression by mononuclear cells of the host which contribute to disease development. In this study, to elucidate the role of these cytokines in chronic adult periodontitis, we tested whether the prevalence of mRNA for inflammatory cytokines generally associated with mononuclear phagocytes was higher in diseased than in healthy gingival tissue. Gingival mononuclear cells or whole gingival biopsies from 32 adult periodontitis patients and five healthy individuals used as controls were evaluated for inflammatory cytokine mRNA expression by reverse-transcription polymerase chain-reaction (RT-PCR) procedures. The cytokines assessed included IL-1 alpha, IL-1 beta, IL-1ra, IL-6, IL-8, IL-12, IL-13, TNF-alpha, TGF-beta, and IFN-gamma. The monocyte/macrophage lipopolysaccharide (LPS) receptor CD14 was also assessed. Results showed that TNF-alpha mRNA was present significantly more frequently in diseased than in healthy biopsies, whereas IL-1 alpha, IL-1 beta, and IL-1ra mRNA were found in most (from 80 to 100%) healthy tissues. Message for CD14 was present in both healthy and diseased tissue samples (100%). This study provides evidence for a major role of TNF-alpha in chronic adult periodontitis. Moreover, our results suggest that the mononuclear cells derived from periodontal tissues have the capacity to respond to components of periodontal pathogens and express both pro- and anti-inflammatory cytokines in these tissues.

This article has been cited by other articles:

				S. Brozovic, R. Sahoo, S. Barve, H. Shiba, S. Uriarte, R. S. Blumberg, and D. F. Kinane Porphyromonas gingivalis enhances FasL expression via up-regulation of NF{kappa}B-mediated gene transcription and induces apoptotic cell death in human gingival epithelial cells. Microbiology, March 1, 2006; 152(Pt 3): 797 - 806. [Abstract] [Full Text] [PDF]

				F.C. Gibson III, H. Yumoto, Y. Takahashi, H.-H. Chou, and C.A. Genco Innate Immune Signaling and Porphyromonas gingivalis-accelerated Atherosclerosis J. Dent. Res., February 1, 2006; 85(2): 106 - 121. [Abstract] [Full Text] [PDF]

				M. Mogi, J. Otogoto, N. Ota, and A. Togari Differential Expression of RANKL and Osteoprotegerin in Gingival Crevicular Fluid of Patients with Periodontitis J. Dent. Res., February 1, 2004; 83(2): 166 - 169. [Abstract] [Full Text] [PDF]

				Y.-T. A. Teng THE ROLE OF ACQUIRED IMMUNITY AND PERIODONTAL DISEASE PROGRESSION Crit. Rev. Oral. Biol. Med., July 1, 2003; 14(4): 237 - 252. [Abstract] [Full Text] [PDF]

				Y. Asai, T. Jinno, and T. Ogawa Oral Treponemes and Their Outer Membrane Extracts Activate Human Gingival Epithelial Cells through Toll-Like Receptor 2 Infect. Immun., February 1, 2003; 71(2): 717 - 725. [Abstract] [Full Text] [PDF]

				Y. Asai, Y. Ohyama, K. Gen, and T. Ogawa Bacterial Fimbriae and Their Peptides Activate Human Gingival Epithelial Cells through Toll-Like Receptor 2 Infect. Immun., December 1, 2001; 69(12): 7387 - 7395. [Abstract] [Full Text] [PDF]

				B. Wang, E. Kraig, and D. Kolodrubetz Use of Defined Mutants To Assess the Role of the Campylobacter rectus S-Layer in Bacterium-Epithelial Cell Interactions Infect. Immun., March 1, 2000; 68(3): 1465 - 1473. [Abstract] [Full Text] [PDF]

				S. Krisanaprakornkit, A. Weinberg, C. N. Perez, and B. A. Dale Expression of the Peptide Antibiotic Human beta -Defensin 1 in Cultured Gingival Epithelial Cells and Gingival Tissue Infect. Immun., September 1, 1998; 66(9): 4222 - 4228. [Abstract] [Full Text] [PDF]