UNLABELLED: The arachidonic acid metabolites prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are inflammatory mediators which are likely to be involved in the pathogenesis of periodontal disease. PGE2 mediates vasodilatation, increases vascular permeability, enhances pain perception by bradykinin and histamine, alters connective tissue metabolism and enhances osteoclastic bone resorption. LTB4 causes the accumulation of inflammatory cells in the inflamed sites, and degranulation of polymorphonuclear leukocytes. OBJECTIVE: To measure gingival crevicular fluid (GCF) levels of PGE2, LTB4 and periodontal health. METHODS: The periodontal condition of 24 subjects was evaluated on the basis of plaque index, gingival index, probing depth, and attachment level. GCF samples were collected from one or two site(s) of each sextant per subject and the volume was measured using Periotron 6000. Samples were then assayed for PGE2 and LTB4 using a competitive enzyme immunoassay. Mean PGE2 and LTB4 levels were determined for each subject and group means compared. RESULTS: Significant differences in the levels of PGE2 and LTB4 were found between patients with periodontitis, and non-periodontitis individuals (P < 0.001). The PGE2/LTB4 levels were positively correlated with the clinical parameters (P < 0.01) and reduced markedly after phase 1 of the periodontal treatment (P < 0.01). The total amount and concentration (ng ml-1) of LTB4 was positively correlated with the gingival index (P < 0.01). CONCLUSIONS: These results indicate that the levels of PGE2 correlated with the severity of the periodontal status, and the levels of LTB4 correlated with gingival inflammation. Thus, our data suggest that the total amounts of PGE2/LTB4 may be good indicators for periodontal inflammation.
UNLABELLED: The arachidonic acid metabolites prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are inflammatory mediators which are likely to be involved in the pathogenesis of periodontal disease. PGE2 mediates vasodilatation, increases vascular permeability, enhances pain perception by bradykinin and histamine, alters connective tissue metabolism and enhances osteoclastic bone resorption. LTB4 causes the accumulation of inflammatory cells in the inflamed sites, and degranulation of polymorphonuclear leukocytes. OBJECTIVE: To measure gingival crevicular fluid (GCF) levels of PGE2, LTB4 and periodontal health. METHODS: The periodontal condition of 24 subjects was evaluated on the basis of plaque index, gingival index, probing depth, and attachment level. GCF samples were collected from one or two site(s) of each sextant per subject and the volume was measured using Periotron 6000. Samples were then assayed for PGE2 and LTB4 using a competitive enzyme immunoassay. Mean PGE2 and LTB4 levels were determined for each subject and group means compared. RESULTS: Significant differences in the levels of PGE2 and LTB4 were found between patients with periodontitis, and non-periodontitis individuals (P < 0.001). The PGE2/LTB4 levels were positively correlated with the clinical parameters (P < 0.01) and reduced markedly after phase 1 of the periodontal treatment (P < 0.01). The total amount and concentration (ng ml-1) of LTB4 was positively correlated with the gingival index (P < 0.01). CONCLUSIONS: These results indicate that the levels of PGE2 correlated with the severity of the periodontal status, and the levels of LTB4 correlated with gingival inflammation. Thus, our data suggest that the total amounts of PGE2/LTB4 may be good indicators for periodontal inflammation.