Cytoskeletal actin reorganization in neutrophils from patients with localized juvenile periodontitis

Localized juvenile periodontitis (LJP) is an early-onset periodontal disease associated with a polymorphonuclear neutrophil (PMN) defective migratory response. Kinetics of actin polymerization-depolymerization determine the shape changes occurring in the plasma membrane-associated cytoskeleton and provide the driving force for directed cell migration (chemotaxis). Therefore, we investigated the relation between an abnormality in LJP PMN chemotaxis and an altered reorganization of the actin filament network. PMNs isolated from peripheral blood of LJP patients (n=14) and matching control subjects (n=12) were evaluated for random and directed migration in a Boyden chamber assay, and the kinetics of actin polymerization were studied by flow cytometry. Three groups of LJP patients could be distinguished on the basis of their PMN-chemotactic response compared to their matched control: depressed (n=6), normal (n=4), and elevated (n=4). The abnormal (depressed or elevated) chemotaxis was generally not related to abnormal random migratory response, except for two patients. Since the kinetics of formyl-methionyl-leucyl-phenylalanine-induced F-actin response were highly variable from one subject to another, means were calculated at each timepoint with the values obtained from each group of subjects and compared by a general factorial design analysis. No statistically significant differences were detected between the control group and the LJP patient group. Furthermore, the data did not show a correlation between the kinetics of actin polymerization-depolymerization and the abnormal chemotactic response observed in LJP PMNs. Hence, the chemotaxis defect in LJP PMN appears to be mediated by signaling events that carry their effect independently of an intact cytoskeleton.