Abstract
The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such as Porphyromonas gingivalis, that accounts for the majority of periodontal tissue damage. Neutrophils are the most abundant leukocytes in periodontal pockets and depending on the stage of the disease, also plentiful PMNs are present in the inflamed gingival tissue and the gingival crevice. They are the most efficient phagocytes and eliminate pathogens by a variety of means, which are either oxygen-dependent or -independent. However, these secretory lethal weapons do not strictly discriminate between pathogens and host tissue. Current studies describe conflicting findings about neutrophil involvement in periodontal disease. On one hand literature indicate that hyper-reactive neutrophils are the main immune cell type responsible for this observed tissue damage and disease progression. Deregulation of neutrophil survival and functions, such as chemotaxis, migration, secretion of antimicrobial peptides or enzymes, and production of reactive oxygen species, contribute to observed tissue injury and the clinical signs of periodontal disease. On the other hand neutrophils deficiencies in patients and mice also result in periodontal phenotype. Therefore, P. gingivalis represents a periodontal pathogen that manipulates the immune responses of PMNs, employing several virulence factors, such as gingipains, serine proteases, lipid phosphatases, or fimbriae. This review will sum up studies devoted to understanding different strategies utilized by P. gingivalis to manipulate PMNs survival and functions in order to inhibit killing by a granular content, prolong inflammation, and gain access to nutrient resources.
Highlights
Reviewed by: George Hajishengallis, University of Pennsylvania, United States Thomas Elliott Van Dyke, The Forsyth Institute, United States
The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such as Porphyromonas gingivalis, that accounts for the majority of periodontal tissue damage
Neutrophil homeostasis in the periodontium is ensured by a balance between neutrophil migration to the site of infection, anti-bacterial and pro-inflammatory response, and the clearance of apoptotic PMNs during the resolution of inflammation
Summary
Reviewed by: George Hajishengallis, University of Pennsylvania, United States Thomas Elliott Van Dyke, The Forsyth Institute, United States. These results indicated that mouse models are certainly very useful tools in analysis of P. gingivalis-mediated periodontal inflammation and in vivo analysis contribute to development targeted therapeutics modulating inflammatory cascades regulated by complement (Hajishengallis and Lambris, 2013), GSK-3 (Adamowicz et al, 2012), regulatory T cells (Glowacki et al, 2013), and neutrophils (Eskan et al, 2012).
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