Abstract
A complex network of chemokines and pro- and anti-inflammatory mediators is involved in the initiation and progression of chronic periodontitis. Matrix metalloproteinases (MMPs), the main enzymes responsible for matrix degradation, are important for periodontal tissue destruction, but their activity can be inhibited by tissue inhibitors of metalloproteinases (TIMPs). Interleukin-12 (IL-12) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have been shown to be involved in inflammatory and autoimmune diseases. Until now, no studies have reported on serum levels of MMP-2 and GM-CSF in chronic periodontitis patients and periodontally healthy subjects. Therefore, the aim of the present study was to determine the serum levels of MMP-2, TIMP-1, IL-12 and GM-CSF in chronic periodontitis patients, compared with periodontally healthy subjects. The test group of the study comprised 40 chronic periodontitis patients, whereas the control group included 108 periodontally healthy individuals. Blood samples were collected from all participants and examined using enzyme-linked immunosorbent assay (ELISA) analysis. Clinical periodontal parameters (bleeding on probing, clinical attachment level and probing pocket depth) and the serum levels of MMP-2, TIMP-1, IL-12 and GM-CSF were statistically significantly higher in the test group than in the conptrol group. These results may indicate that MMP-2, TIMP-1, IL-12 and GM-CSF could be involved in the initiation and progression of chronic periodontitis. Key words: Chronic periodontitis, cytokines, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-1 (TIMP-1), interleukin-12 (IL-12), granulocyte–macrophage colony-stimulating factor (GM-CSF).
Highlights
Periodontitis is a multifactorial infection characterized by a destructive inflammatory process affecting toothsupporting tissues and resulting in periodontal pocket formation and alveolar bone resorption, which might eventually lead to tooth loss (Armitage, 1999; Cazalis et al, 2009)
There was no occurrence of gingival recession and clinical attachment loss (CAL) in the control group, while 32.14 ± 3.7% patients accounted for gingival recession and the mean CAL was 5.9 ± 2.45 mm in the periodontitis group (Table 1)
Statistically significant differences in the serum levels of Matrix metalloproteinase-2 (MMP-2), tissue inhibitors of metalloproteinases (TIMPs)-1, IL-12 and granulocyte-macrophage colony-stimulating factor (GM-CSF) were demonstrated between the two groups (p < 0.001; Table 2)
Summary
Periodontitis is a multifactorial infection characterized by a destructive inflammatory process affecting toothsupporting tissues and resulting in periodontal pocket formation and alveolar bone resorption, which might eventually lead to tooth loss (Armitage, 1999; Cazalis et al, 2009). The continuous challenge of host immune and resident cells by periodontopathogens and their virulence factors results in a complex network of pro- and anti-inflammatory cytokines acting in the inflamed periodontal tissues (Okada and Murakami, 1998). These host mediators directly or indirectly participate in periodontal tissue destruction and in bone resorption (Birkedal-Hansen, 1993a). MMPs can be inhibited by a family of naturally occurring specific inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), which are essential in maintaining a dynamic equilibrium in connective tissue metabolism (Brew et al, 2000; Spinale, 2002)
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