Publication | Open Access
Neutrophil Dysfunctions, IL-8, and Soluble L-Selectin Plasma Levels in Rapidly Progressive Versus Adult and Localized Juvenile Periodontitis: Variations According to Disease Severity and Microbial Flora
44
Citations
45
References
1999
Year
InflammationPeriodontologyPeriodontal DiseaseLocalized Juvenile PeriodontitisGranulocyteDisease SeverityPathogenesisImmunologyProgressive Versus AdultInflammatory MarkerOral MicrobiologyVascular BiologyMedicineAdult PeriodontitisClinical MicrobiologyProgressive PeriodontitisOxidative Stress
We used flow cytometry to analyze the expression of adhesion molecules and the oxidative burst of whole-blood polymorphonuclear neutrophils (PMN) from 26 patients with periodontitis. Three different clinical entities were studied: adult periodontitis (AP), localized juvenile periodontitis (LJP), and rapidly progressive periodontitis (RPP). Unstimulated PMN from the patients showed reduced Lewis x, sialyl-Lewis x, and L-selectin expression relative to those from healthy control subjects. These alterations were present whatever the severity of periodontal disease. However, PMN from RPP patients showed increased basal H2O2 production and decreased L-selectin shedding. These latter impairments, which correlated with increased IL-8 plasma levels, could contribute to initial vascular damage. In addition, decreased IL-8 priming of H2O2 production by PMN from RPP patients could account for a lower bactericidal capacity of PMN, leading to the large number of bacteria in the subgingival region of RPP patients. Soluble L-selectin plasma levels were also decreased in the RPP group, indicating more severe or diffuse endothelial damage. These abnormalities were not found in the patients with less destructive forms of periodontitis (AP and LJP). Porphyromonas gingivalis, a bacterial pathogen known to increase IL-8 production by PMN, was found in the periodontal pockets of RPP patients only. These results show links among PMN abnormalities, the clinical form of periodontitis, and the gingival bacterial flora.
| Year | Citations | |
|---|---|---|
Page 1
Page 1