Several studies have documented suppressed polymorphonuclear neutrophil (PMN) chemotaxis in most patients with juvenile periodontitis. In contrast, data regarding PMN chemotaxis in patients with rapidly progressive periodontitis are very limited, and monocyte (MN) chemotaxis and random migration of PMNs or MNs from these patients have not been studied previously. Accordingly, we examined cell motility of PMNs and MNs from 27 patients with rapidly progressive periodontitis, 5 patients with juvenile periodontitis, and 37 normal control subjects by using a microchamber technique and the synthetic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP) as the chemoattractant. As a group, PMNs and MNs from patients with rapidly progressive periodontitis manifested significantly enhanced random migration relative to control cells (P less than 0.001), suppressed directed migration (chemotaxis) at FMLP doses of 10(-9) and 10(-8) M (P less than 0.05), and enhanced directed migration at a dose of 10(-6) M FMLP (P less than 0.01). In contrast, PMNs from patients with juvenile periodontitis exhibited normal random migration, and directed migration was significantly suppressed at all doses of FMLP tested (P less than 0.05). An abnormality of either PMN or MN motility was observed in 26 of 27 patients with rapidly progressive periodontitis. Enhanced random migration was seen in PMNs in 63%, MNs in 39%, and both cell types in 26% of the patients. Suppressed chemotaxis was seen in PMNs in 85%, in MNs in 74%, and in both cell types in 69% of the patients. The prevalence and magnitude of abnormalities in motility were somewhat lower in treated than in untreated patients. Thus, most, if not all, of this subgroup of patients with early onset, highly destructive periodontitis have abnormalities in PMN or MN motility, and these defects may differ from those seen in cells from patients with the juvenile form of the disease.
Previous reports have suggested that aflatoxin B1 (AFB1) is a membrane-active compound capable of mediating chromosomal damage through release of toxic oxygen radicals and arachidonic acid metabolites by human leukocytes. Thus, the ability of AFB1 to stimulate directly arachidonic acid metabolism and generate a respiratory burst in human neutrophils and monocytes was examined. AFB1 (10(-8)-10(-6) M) failed to induce [3H]arachidonate release from prelabeled human neutrophils or mononuclear leukocytes. Similarly AFB1 exposure at these concentrations failed to stimulate the production of either thromboxane (TX)B2 or leukotriene (LT)B4 from adherent monocytes. AFB1 was also ineffective in stimulating respiratory burst activity as measured by superoxide anion (O2.-) formation in both neutrophil and mononuclear leukocytes. We conclude that AFB1 is unable to stimulate either arachidonic acid metabolism or initiate a respiratory burst of human leukocytes. Therefore, it appears that these pathways are not involved in the genotoxic mechanisms of AFB1 as previously suggested.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.