Levels of platelet-activating factor in gingival crevicular fluid and gingival tissue in specific periodontal diseases.

Abstract

Platelet-activating factor (PAF), a potent phospholipid mediator of inflammatory and immune reactions, is involved in a variety of biological responses seen in periodontal diseases. The aim of the present study was to examine the role of PAF in the pathogenesis of specific periodontal diseases. PAF levels were investigated in gingival crevicular fluid (GCF) and gingival tissue (GT) samples of 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 10 patients with chronic periodontitis (CP), 6 with gingivitis (G), and 6 periodontally healthy subjects (H). Periodontal status was evaluated by measuring probing depth, gingival index, papillary bleeding index, and plaque index. PAF was extracted from GCF samples passing through amberlit resin columns, purified by high performance liquid chromatographic method, and then analyzed by radioimmunoassay. GAgP, LAgP, and CP groups had significantly higher GCF PAF levels compared to the H group (P<0.005). Although statistically not significant, GCF PAF levels were also higher in the G group than those of the H group (P = 0.0784). GAgP, LAgP, and CP groups had similar GCF PAF levels (P>0.005). These groups had higher levels of GCF PAF than those of the G group, but the difference was significant only for the GAgP group (P<0.005). When the data were expressed as concentration, GAgP, LAgP, and CP groups were found to have higher concentrations of GCF PAF compared to the H group (P<0.005). GCF PAF concentration was similar in patient groups (P>0.005). All patient groups had significantly higher GT PAF levels compared to the H group (P<0.005). GAgP, LAgP, and CP groups had similar amounts of GCF and GT PAF (P>0.005). GAgP, LAgP, and CP groups had higher GT PAF levels than those of the G group, but the differences were only significant for LAgP and CP groups (P<0.005). No significant correlation was found between GCF and GT PAF levels and clinical parameters. The results of the present study indicate that PAF is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. To our knowledge, this is the first report investigating PAF levels in GCF and GT in specific periodontal diseases. We believe that this potent phospholipid mediator may need to be considered in the pathogenesis of periodontal diseases.