scholarly journals Porphyromonas gingivalis proteinases in periodontitis, a review.

1996 ◽  
Vol 43 (3) ◽  
pp. 455-465 ◽  
Author(s):  
J Potempa ◽  
J Travis
Keyword(s):  
Porphyromonas Gingivalis ◽  
Catalytic Domain ◽  
Gingival Crevicular Fluid ◽  
Proteolytic Enzymes ◽  
Periodontal Diseases ◽  
Proteolytic Processing ◽  
Tissue Destruction ◽  
Single Chain ◽  
Neutrophil Accumulation ◽  
Crevicular Fluid

Porphyromonas gingivalis has been closely associated with the initiation and progression of some forms of periodontal diseases and its proteolytic enzymes have been implicated in invasion, tissue destruction and evasion of host antibacterial defenses. Recently, the primary focus of research has been on cysteine proteinases, referred to as gingipain R and gingipain K which are produced in large quantities and are directly involved in pathological events during development and progression of periodontitis, contributing to clinical hallmarks of the disease including: flow of gingival crevicular fluid, neutrophil accumulation and bleeding on probing. Gingipain R exists as 110-, 95-, 70- to 90- and 50-kDa proteins, the first two being a complex of the 50-kDa catalytic subunit with hemagglutinin/adhesins, with or without an added membrane anchorage peptide. The other forms are single-chain enzymes. The predominant form of gingipain K in P. gingivalis strains is a complex of a 60-kDa catalytic protein with hemagglutinin/adhesins. Molecular cloning and structural characterization of the gingipain R and gingipain K genes has shown that they code for 1704 and 1722 amino-acid residue preproenzymes, respectively. Although both structures show no similarity within the preprofragment and only limited identity within the catalytic domain (27%) they are essentially identical within the putative hemagglutinin/adhesin domain. Furthermore, on the basis of gene structure it is now apparent that various soluble and membrane bound forms of gingipains are derived through proteolytic processing of the preproenzymes, and it can be assumed that the Arg-X-specific enzyme is responsible for this processing.

scholarly journals Porphyromonas gingivalis Fimbria-Induced Expression of Inflammatory Cytokines and Cyclooxygenase-2 in Mouse Macrophages and Its Inhibition by the Bioactive Compounds Fibronectin and Melatonin

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Yukio Murakami ◽  
Mamoru Machino ◽  
Seiichiro Fujisawa
Keyword(s):  
Porphyromonas Gingivalis ◽  
Bioactive Compounds ◽  
Gingival Crevicular Fluid ◽  
Current Knowledge ◽  
Periodontal Diseases ◽  
Oral Bacteria ◽  
Cyclooxygenase 2 ◽  
Nf Kappa B ◽  
Mouse Macrophages ◽  
Crevicular Fluid

Porphyromonas gingivalis (Pg) fimbriae, in addition to lipopolysaccharide, are involved in the pathogenesis of periodontal disease. At the same time, bioactive compounds such as fibronectin (FN) and melatonin in saliva and gingival crevicular fluid have been reported to exert a preventive effect against periodontitis. Here, we review current knowledge regarding the potent inhibitory effects of FN and melatonin against Pg fimbria-induced induction of proinflammatory cytokines, cyclooxygenase-2 (COX-2) expression, and NF-kappa B activation in mouse macrophages and discuss their possible clinical application for prevention of periodontal diseases induced by oral bacteria.

Salivary Diagnosis - Clinical Uses in Assessing Oral Inflammation

2017 ◽  
Vol 68 (6) ◽  
pp. 1201-1204 ◽  
Author(s):  
Iulia Ioana Stanescu ◽  
Alexandra Totan ◽  
Florentina Rus ◽  
Daniela Miricescu ◽  
Brandusa Mocanu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Periodontal Disease ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Marker ◽  
Clinical Settings ◽  
Tissue Destruction ◽  
Whole Saliva ◽  
Oral Inflammation ◽  
Positive Correlations ◽  
Crevicular Fluid

The past decades demonstrated that saliva and its components represent a remarkable diagnosis fluid with valuable clinical uses for both oral and systemic diseases. At the same time it is well established that oxidative stress is involved in a wide number of pathologies, including periodontitis. The specific aim of the present study which included 50 subjects is to determine if saliva can be used in clinical settings to correlate oxidative stress and tissue destruction markers with the severity of periodontal disease. An important oxidative stress marker - 8-hydroxydesoxyguanosine (8-OHdG) and a collagen degradation marker - beta-crosslaps (b-CTX) were quantified in both saliva and gingival crevicular fluid (GCF) using ELISA kits and were found to be significantly increased in the chronic periodontitis group when compared to respective controls (p[0.05). At the same time positive correlations were observed between whole saliva and gingival crevicular fluid (p[0.05). Significant correlations were also determined between GCF and salivary markers and clinical parameters of periodontal disease. Present results demonstrate that saliva and its components can successfully be used in clinical settings and represents a reliable tool for assessing periodontal disease severity.

scholarly journals Are Proteinase 3 and Cathepsin C Enzymes Related to Pathogenesis of Periodontitis?

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Oya Türkoğlu ◽  
Elif Azarsız ◽  
Gülnur Emingil ◽  
Necil Kütükçüler ◽  
Gül Atilla
Keyword(s):  
Gingival Crevicular Fluid ◽  
Periodontal Diseases ◽  
Study Groups ◽  
Aggressive Periodontitis ◽  
Control Group ◽  
Proteinase 3 ◽  
Cathepsin C ◽  
Probing Depth ◽  
Inflammatory Processes ◽  
Crevicular Fluid

Aim. Cathepsin C is the activator of the polymorphonuclear leukocyte-derived proteinase 3, which contributes to inflammatory processes. The aim of the present study was to investigate gingival crevicular fluid (GCF) proteinase 3 and cathepsin C levels in periodontal diseases.Design. Eighteen patients with chronic periodontitis (CP), 20 patients with generalized aggressive periodontitis (G-AgP), 20 patients with gingivitis, and 18 healthy subjects were included in the study. Periodontal parameters including probing depth, clinical attachment level, papilla bleeding index, and plaque index were assessed in all study subjects. GCF proteinase 3 and cathepsin C levels were analyzed by ELISA.Results. GCF proteinase 3 total amount was significantly higher in diseased groups compared to control group, after adjusting ageP<0.05. No differences were found in GCF cathepsin C levels among the study groupsP>0.05. Periodontal parameters of sampling sites were positively correlated with GCF proteinase 3 total amountsP<0.01but not with cathepsin C total amountsP>0.05.Conclusions. Elevated levels of GCF proteinase 3 in CP, G-AgP, and gingivitis might suggest that proteinase 3 plays a role during inflammatory periodontal events in host response. However, cathepsin C in GCF does not seem to have an effect on the pathogenesis of periodontal diseases.

Diagnosis of Periodontal Diseases: Reaction Paper

1991 ◽  
Vol 5 (1) ◽  
pp. 37-40 ◽  
Author(s):  
M.J. Novak
Keyword(s):  
Gingival Crevicular Fluid ◽  
Periodontal Diseases ◽  
Diagnostic Techniques ◽  
Disease States ◽  
Specificity And Sensitivity ◽  
Biochemical Analyses ◽  
Clinical Measurements ◽  
The Individual ◽  
Crevicular Fluid ◽  
Technological Improvements

With the recent description of 12 different forms and sub-forms of periodontitis by the World Workshop in Clinical Periodontics (1989), increased emphasis has been placed on diagnosis. Dr. Ranney's review addressed the specificity and sensitivity of current diagnostic tests with respect to their ability to differentiate between health and disease and between the individual disease states. Although considerable microbiologic and immunologic data have been accumulated in the past decade, very little of this information has proved to be sufficiently sensitive to be of use in differential diagnosis. Clinical measurements provide us with an insensitive, retrospective analysis of what has already occurred but allow us to diagnose disease based on its natural history. Measures of attachment levels, by use of conventional probes, are only sufficiently sensitive indicators of periodontitis when as much as 20-30% of attachment has already been lost. Current technological improvements in probing measurements and radiographic assessment may increase sensitivity in this area. Future improvements in diagnostic techniques will occur with the advent of sensitive biochemical analyses of gingival crevicular fluid. These assays will provide a more objective analysis of inflammation and, in time, will provide sufficient sensitivity to allow for differentiation between and among the various forms of periodontal disease. Future directions in diagnosis will focus on the identification of disease-susceptible individuals and the prediction of future periodontal breakdown.

scholarly journals Host Mediators in Gingival Crevicular Fluid: Implications for the Pathogenesis of Periodontal Disease

1992 ◽  
Vol 3 (1) ◽  
pp. 31-60 ◽  
Author(s):  
Ira B. Lamster ◽  
M. John Novak
Keyword(s):  
Immune Response ◽  
Periodontal Disease ◽  
Gingival Crevicular Fluid ◽  
Critical Role ◽  
Arachidonic Acid Metabolite ◽  
Reactive Oxygen Metabolites ◽  
Tissue Destruction ◽  
Crevicular Fluid ◽  
Relationship Of ◽  
The Relationship

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes P-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-la, IL-1β, tumor necrosis factor-a), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1β and TNF-a, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.

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