Differential platelet‐activating factor synthesis by monocytes and polymorphonuclear leukocytes from subjects with localized aggressive periodontitis

Background and Objective:  Platelet‐activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet‐activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet‐activating factor acetylhydrolase, the enzyme that catabolizes platelet‐activating factor. The objective of this study was to determine if platelet‐activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet‐activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis. Material and Methods:  Cells were labeled with [ 3 H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet‐activating factor was extracted and quantified by scintillation counting. Results:  For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet‐activating factor, and calcium ionophore A23187 stimulated platelet‐activating factor production in both cell types. However, calcium ionophore A23187‐activated monocytes from subjects with localized aggressive periodontitis produced less platelet‐activating factor than did activated periodontally healthy monocytes ( p  < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet‐activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet‐activating factor synthesis, whereas calcium ionophore A23187‐stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced ≈ 12 times more platelet‐activating factor than did resting monocytes. In contrast, both resting and activated localized aggressive periodontitis polymorphonuclear neutrophils synthesized more platelet‐activating factor than did periodontally healthy polymorphonuclear neutrophils. Conclusion:  These data suggest that high levels of platelet‐activating factor in subjects with localized aggressive periodontitis result from both increased synthesis and reduced catabolism. While localized aggressive periodontitis polymorphonuclear neutrophils contribute to increased platelet‐activating factor mass through synthesis, the contribution of monocytes is probably the result of reduced catabolism by platelet‐activating factor acetylhydrolase.