ISSN:
1600-0765
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Background: Human periodontal diseases are inflammatory disorders that are the result of complex interactions between periodontopathogens and the host's immune response. Two important and interrelated factors are involved in the pathophysiological progression of periodontal diseases, i.e. the activation of immune system and the production of oxygen radicals and their related metabolites. Increased production of oxygen radicals may contribute to oxidative stress, which is reported to be involved in many diseases, including periodontal diseases.Objectives: The objective of this study was to investigate glutathione peroxidase, lactoferrin and myeloperoxidase, which play an essential role in free radical production and defenses, and the proinflammatory cytokine interleukin-1β (IL-1β), which is important in the regulation of immunological and inflammatory reactions in human periodontal diseases.Methods: Gingival crevicular fluid (GCF) samples were collected from 27 subjects, 19 periodontitis patients and eight healthy controls, ranging in ages from 24 to 62 years. Clinical parameters were recorded. GCF glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1β were analyzed by enzyme-linked immunosorbent assays (ELISA).Results: The periodontitis sites exhibited significantly greater total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1β than healthy sites. Total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1β was positively correlated with plaque index, gingival index, probing depth and probing attachment level (p 〈 0.05).Conclusion: The imbalance between the levels of myeloperoxidase/IL-1β and glutathione peroxidase/lactoferrin could result in tissue damage of reactive oxygen species (ROS) in periodontitis which is initiated and perpetuated by the chronic insults of periodontopathogens.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-0765.2004.00744.x
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