Neutrophil Defects and Host-Parasite Interactions in the Pathogenesis of Localized Juvenile Periodontitis

Abstract

Through the study of host responses in periodontal diseases, the role of the neutrophil as an important protective cell in the pathogenesis of disease has become apparent. In this report, we examine the neutrophil defects associated with localized juvenile periodontitis to include defects of cell surface protein expression, defects of signal transduction, and defects of bactericidal activity. We report that LJP neutrophils are deficient in chemotactic factor receptors and a chemotaxis-related glycoprotein (GP110). There is a deficit of signal transduction, resulting in a decrease in leukotriene B4 production, and the LJP neutrophil is deficient in its ability to kill the periodontal pathogen, Actinobacillus actinomycetemcomitans. The study of neutrophil biology in the LJP model and the application of these studies to the more prevalent disease, adult periodontitis, are discussed.