Document Type : Original Article

Authors

1 Department of Periodontology, School of Dentistry, Mashhad University of Medical Sciences, Mashhad, Iran.

2 Mashhad Dental Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran.

3 Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

4 Department of Periodontology, School of Dentistry, Ghazvin University of Medical Sciences, Ghazvin, Iran.

10.22034/iji.2008.48559

Abstract

Background: Several cytokines, including IL-6 have been implicated in the pathogenesis of periodontal disease. It is established that monocytes from periodontitis subjects show an increased production of IL-6 as compared to healthy subjects. However, little is known about the effect of periodontal treatment on IL-6 production by monocytes in subsets of periodontitis patients. Objective: The aim of the present study was to evaluate the effect of surgical periodontal treatment on IL-6 production of peripheral blood monocytes (PBM) in aggressive periodontitis patients (AP) and chronic periodontitis patients (CP) before and after stimulation by E.coli LPS. Methods: Fifteen AP patients, 15 CP patients and 15 periodontally healthy subjects (PH) took part in the study. PBM IL-6 pro-duction was measured, using ELISA, before and after stimulation of cultured PBM cells by 0.1 microg/ml LPS of E.coli. Following full-mouth non-surgical and surgical periodontal treatment of the AP and CP groups, the same measurements were repeated for these two groups. Results: LPS-stimulated IL-6 production was significantly greater than non-stimulated IL-6 for all 3 groups. Before periodontal treatment, LPS-stimulated IL-6 pro-duction of the AP group was significantly greater than the other 2 groups. Periodontal treatment did not result in a significant decrease in unstimulated or LPS-stimulated IL-6 production by PBM cells in AP and CP patients. No correlation was detected between IL-6 levels and baseline clinical parameters or changes in clinical parameters. Conclusion: PBM cells in AP patients might be hyper-responsive in terms of IL-6 production. This hyper-responsiveness does not seem to return to that of healthy subjects even after a successful periodontal treatment. Moreover, the regulation of host inflammatory mechanisms upon LPS challenge might be different between AP and CP patients.

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