4.6 Article

Characterization of progressive periodontal lesions in chronic periodontitis patients: levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells

Journal

JOURNAL OF CLINICAL PERIODONTOLOGY
Volume 35, Issue 3, Pages 206-214

Publisher

WILEY
DOI: 10.1111/j.1600-051X.2007.01190.x

Keywords

cytokines; inflammatory cells; matrix metalloproteinases; periodontal pathogens; progressive periodontitis

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Background and aims: Periodontitis is an infection with an episodic nature of tissue support destruction. The aim of this work was to determine the levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells in periodontal sites characterized by active periodontal connective tissue destruction. Material and Method: Fifty-six patients with moderate or advanced severity of chronic periodontitis were selected. Periodontitis was characterized by at least six sites with probing depth >= 5 mm, clinical attachment level >= 3 mm and radiographic bone loss. Periodontitis progression was determined by the tolerance method. Receptor activator for nuclear factor kappa B-ligand (RANK-L), monocyte chemoattractant protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha), IL-1 beta, MMP-13, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsithia and inflammatory cells levels were determined. Statistical analysis was performed using the Stata((R)) 7.0 software. Data were expressed as mean +/- SD and paired samples t-test and chi(2) tests were used. Results: Higher RANK-L, IL-1 beta and MMP-13 activity levels were observed in active sites (p < 0.05). The proportion of P. gingivalis, A. actinomycetemcomitans, T. forsythia and the number of CD4(+) T were higher in active than in inactive sites (p > 0.05). Conclusion: The detection of periodontopathic bacteria, host matrix metalloproteinases and cytokines in periodontitis patients with lesions undergoing episodic attachment loss could partially explain the mechanisms associated with the destruction of the supporting tissues of the tooth.

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