An alteration of the immune system function is one of the main factors involved in the development of periodontal disease. Polymorpho-nuclear neutrophil leukocytes (PMN) play a crucial role in the cell-mediated immune response against bacterial challenge. The mechanism of neutralization of pathogen microorganisms by PMNs involves many different steps: adhesion to capillary endothelium in the inflamed region, trans-endothelial migration, chemotaxis, phagocytosis and, ultimately, bacterial killing by oxidative and non-oxidative mechanisms. A defect in one of these steps leads to altered neutrophil function and, consequently, to a higher host susceptibility to periodontal tissue infection. The main intrinsic neutrophil diseases such as neutropenia, leukocyte adhesion deficiency (LAD-1), Chediak-Higashi syndrome, Papillon-Lefèvre syndrome, chronic granulomatous disease (CGD), are often related to severe and early-onset forms of periodontitis, as described by many evidences in the literature. Therefore PMN dysfunctions, both intrinsic and extrinsic, represent an important risk factor for periodontal disease. Studies on the basic molecular mechanisms of such dysfunctions, also in terms of genetic polymorphisms, recently allowed to identify some specific markers related to a higher susceptibility to the development of disease. Many researches have yet to be performed aiming to gain insight on the dynamics of PMN activation and interaction with other cells, in order to improve and modulate neutrophil function and to develop specific approaches for care and prevention of periodontal diseases.
"The persistence of a local chronic host response may alter the protective roles of inflammatory cells and have deleterious effects on tissues   . In fact, the hyperactivity of neutrophils is associated with periodontal tissue destruction  . Further, it has also been reported that chronic inflammatory conditions often result from the aberrant production of chemokines such as IL-8 . "
[Show abstract][Hide abstract] ABSTRACT: Epithelial cells function as mechanical barriers against invasion by pathogenic organisms and promote intercellular communication through cell–cell junction complexes. Therefore, the permeability of the gingival epithelial cell layer indicates a defensive capability against invasion by periodontal pathogens. Accumulation of activated neutrophils is thought to be involved in the onset of inflammation. Here, we review the effects of irsogladine maleate, a medication for gastric ulcers, on E-cadherin and chemokine expression in gingival epithelial cells exposed to periodontopathogenic bacteria, in order to examine the clinical efficacy of irsogladine maleate in preventing periodontal inflammation.
Journal of Oral Biosciences 05/2012; 54(2):79–82. DOI:10.1016/j.job.2012.02.001
"In fact, defective function of PMNs is associated with severe forms of periodontal diseases. In contrast, the hyperactivity of this cell type is associated with periodontal tissue destruction (Attström, 1975; Del Fabbro et al., 2000; Waddington et al., 2000). In contrast to IL-8/CXCL8, the chemokine MCP-1/CCL2 was found to be preferentially expressed in diseased periodontal sites, and presents a differential spatial distribution in the periodontal tissues, since it is expressed along the basal layer of the oral epithelium and by endothelial cells, fibroblasts, and mononuclear phagocytes in the inflammatory infiltrate (Tonetti et al., 1994; Yu and Graves, 1995). "
[Show abstract][Hide abstract] ABSTRACT: The inflammatory oral diseases are characterized by the persistent migration of polymorphonuclear leukocytes, monocytes, lymphocytes, plasma and mast cells, and osteoblasts and osteoclasts. In the last decade, there has been a great interest in the mediators responsible for the selective recruitment and activation of these cell types at inflammatory sites. Of these mediators, the chemokines have received particular attention in recent years. Chemokine messages are decoded by specific receptors that initiate signal transduction events, leading to a multitude of cellular responses, including chemotaxis and activation of inflammatory and bone cells. However, little is known about their role in the pathogenesis of inflammatory oral diseases. The purpose of this review is to summarize the findings regarding the role of chemokines in periapical and periodontal tissue inflammation, and the integration, into experimental models, of the information about the role of chemokines in human diseases.
Journal of Dental Research 05/2007; 86(4):306-19. DOI:10.1177/154405910708600403 · 4.14 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Localized aggressive periodontitis (LAgP) is a disease characterized by rapid loss of alveolar bone in teeth of otherwise healthy patients. Neutrophils from LAgP patients have been shown to exhibit diminished chemotaxis and low levels of formyl peptide receptor (FPR) surface expression. A recent study has associated LAgP with 2 polymorphisms in the FPR: 110Phe-->Ser and 126Cys-->Trp.
We transfected Chinese hamster ovary cells with wtFPR, FPR-110Phe-->Ser, FPR-126Cys-->Trp, or FPR-110Phe-->Ala and determined their surface expression of FPR, their ligand binding affinity, their G-protein coupling, and their chemotaxis toward N-formyl-methionyl-leucyl-phenylalanine (FMLP).
FPR-110Phe-->Ser mutants failed to show any significant surface expression or chemotaxis toward FMLP. FPR-126Cys-->Trp mutants exhibited slightly lower than normal binding affinity, markedly lower G-protein coupling response, and markedly lower chemotaxis toward FMLP than that observed with wtFPR. We also analyzed another FPR-Phe110 mutant, FPR-110Phe-->Ala, to ascertain what the effect of mutating this residue might be in a mutant that could be expressed on the cell surface. The FPR-110Phe-->Ala mutant demonstrated markedly lower surface expression, normal ligand binding affinity, markedly lower G-protein coupling, and markedly lower chemotaxis toward FMLP.
Our data substantiate the hypothesis that the chemotactic defects observed in LAgP patients are due at least in part to molecular alterations in the FPR. The FPR-110Phe-->Ser polymorphism appears to be more defective than the FPR-126Cys-->Trp polymorphism, indicating that patients with the former polymorphism might be expected to exhibit a more severe form of aggressive periodontitis.
Journal of Periodontology 04/2003; 74(4):475-84. DOI:10.1902/jop.2003.74.4.475 · 2.71 Impact Factor
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