Mediators of Inflammation

Mediators of Inflammation / 2007 / Article

Research Article | Open Access

Volume 2007 |Article ID 038210 | https://doi.org/10.1155/2007/38210

Ivana Brekalo Pršo, Willy Kocjan, Hrvoje Šimic, Gordana Brumini, Sonja Pezelj-Ribaric, Josipa Borcic, Silvio Ferreri, Ivana Miletic Karlovic, "Tumor Necrosis Factor-Alpha and Interleukin 6 in Human Periapical Lesions", Mediators of Inflammation, vol. 2007, Article ID 038210, 4 pages, 2007. https://doi.org/10.1155/2007/38210

Tumor Necrosis Factor-Alpha and Interleukin 6 in Human Periapical Lesions

Received24 Aug 2006
Revised06 Nov 2006
Accepted08 Nov 2006
Published27 Dec 2006

Abstract

Aim. The aim of this study was to evaluate the presence of the cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in human periapical lesions. Subjects and methods. Samples were obtained from three groups of teeth: symptomatic teeth, asymptomatic lesions, and uninflamed periradicular tissues as a control. Results. TNF-alpha levels were significantly increased in symptomatic lesions compared to control. Group with asymptomatic lesions had significantly higher concentrations compared to control. There were no significant differences in TNF-alpha levels between symptomatic and asymptomatic lesions. In group with symptomatic lesions, IL-6 levels were significantly higher than in group with asymptomatic lesions. The IL-6 levels in symptomatic group also showed significantly higher concentration in comparison with control group. In asymptomatic group, the IL-6 level had significantly higher concentrations compared to control. Conclusion. These results indicate that symptomatic lesions represent an immunologically active stage of disease, and asymptomatic lesions are the point from which the process advances toward healing.

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Copyright © 2007 Ivana Brekalo Pršo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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