Clinical and Biochemical Assessment of Interleukin-18 Level in Gingival Crevicular Fluid in chronic and aggressive periodontitis Patients

Abstract

SUMMARY P eriodontal disease is one of the two major dental diseases that affect human populations worldwide (Papapanou, 1999; Petersen and Ogawa, 2005). This pathology includes the inflammatory disorders of gingivitis and periodontitis, which are caused by specific pathogens, such as Porphyromonas gingivalis, Tannerella forsythia and Aggregatibacter actinomycetemcomitans, in the bacterial biofilm that forms adjacent to teeth on a daily basis. These pathogens have been implicated as etiological agents and are associated with the progressive form of the disease (Seymour, 1991; Pihlstrom et al., 2005 and Van Dyke and Sheilesh, 2005). Periodontal diseases are a group of disorders with different etiologies and clinical manifestations. They include periodontitis, which is distinguished by a strong inflammatory response. Two main forms of periodontitis are identified; chronic (CP) and aggressive (AP), and they are characterized by attachment loss, bone destruction, periodontal pockets and gingival inflammation. However, attachment loss and tissue destruction is faster in AP than CP (Lang et al., 1999; Lindhe et al., 1999). It has been reported than IL-18 levels were found to be locally higher in both gingival tissue biopsies and GCF of patients with periodontitis compared with patients with gingivitis and HS (Orozco et al., 2006, Figueredo et al., 2008 and Pradeep et al., 2009). Similar results have been observed in serum (Orozco et al., 2006). Moreover, it has been observed an increase of IL-18 in gingival biopsy tissues correlates directly with the pocket deep (Johnson and Serio, 2005). Several studies, mainly of GCF, have shown that levels of IL-18 in patients with periodontitis differ from those in HS and patients with gingivitis. Interleukin-18 (IL-18) is a proinflammatory cytokine of the IL-1 super family and was originally identified as interferon-γ (IFN-γ) inducing factor. It is unique in having a capacity to induce either Th1 or Th2 differentiation, depending on the immunological context (Nakanishi et al., 2001). It is expressed by macrophages/monocytes and oral epithelial cells, and upregulated in various chronic diseases including periodontal disease. IL-18 could play an important role in gingival inflammation, as relatively high expression of IL- 18 has been found in gingival samples with increasing sulcular depth (Johnson and Serio, 2005). It has been shown that the levels of IL-18 in gingival crevicular fluid (GCF) are increased at sites of both gingivitis and periodontitis, suggesting an association between the severity of periodontal disease and the level of IL-18 (Orozco et al., 2006). The present study was conducted on 40 individuals; 10 chronic periodontitis patients, 10 Localized aggressive periodontitis patients and 10 Generalized aggressive periodontitis and 10 healthy controls. Chronic periodontitis patients included males and females with a