scholarly journals Subgingival Plaque Bacteria and Inflammatory Mediators in Gingival Crevicular Fluid in High-risk Groups for Periodontal Disease.

1994 ◽  
Vol 36 (4) ◽  
pp. 847-856
Author(s):  
Masahiro KITAMURA ◽  
Yasuo MIKI ◽  
Takenori NOZAKI ◽  
Yousuke MORITANI ◽  
Yutaka KUSUMOTO ◽  
...  
Keyword(s):  
High Risk ◽  
Periodontal Disease ◽  
Inflammatory Mediators ◽  
Gingival Crevicular Fluid ◽  
Risk Groups ◽  
Subgingival Plaque ◽  
Crevicular Fluid

Neutrophil pseudoplatelets in subgingival plaque and crevicular fluid samples from periodontal diseased sites

1989 ◽  
Vol 47 ◽  
pp. 862-863 ◽  
Author(s):  
J Hanker ◽  
E.J. Burkes ◽  
G. Greco ◽  
R. Scruggs ◽  
B. Giammara
Keyword(s):  
Electron Microscopy ◽  
Bone Marrow ◽  
Peripheral Blood ◽  
Gingival Crevicular Fluid ◽  
Light And Electron Microscopy ◽  
Subgingival Plaque ◽  
Staining Reaction ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Crevicular Fluid

The mature neutrophil with a segmented nucleus (usually having 3 or 4 lobes) is generally considered to be the end-stage cell of the neutrophil series. It is usually found as such in the bone marrow and peripheral blood where it normally is the most abundant leukocyte. Neutrophils, however, must frequently leave the peripheral blood and migrate into areas of infection to combat microorganisms. It is in such areas that neutrophils were first observed to fragment to form platelet-size particles some of which have a nuclear lobe. These neutrophil pseudoplatelets (NPP) can readily be distinguished from true platelets because they stain for neutrophil myeloperoxidase. True platelets are not positive in this staining reaction because their peroxidase Is inhibited by glutaraldehyde. Neutrophil pseudoplatelets, as well as neutrophils budding to form NPP, could frequently be observed in peripheral blood or bone marrow samples of leukemia patients. They are much more prominent, however, in smears of inflammatory exudates that contain gram-negative bacteria and in gingival crevicular fluid samples from periodontal disease sites. In some of these samples macrophages ingesting, or which contained, pseudoplatelets could be observed. The myeloperoxidase in the ingested pseudoplatelets was frequently active. Despite these earlier observations we did not expect to find many NPP in subgingival plaque smears from diseased sites. They were first seen by light microscopy (Figs. 1, 3-5) in smears on coverslips stained with the PATS reaction, a variation of the PAS reaction which deposits silver for light and electron microscopy. After drying replicate PATS-stained coverslips with hexamethyldisilazane, they were sputter coated with gold and then examined by the SEI and BEI modes of scanning electron microscopy (Fig. 2). Unstained replicate coverslips were fixed, and stained for the demonstration of myeloperoxidase in budding neutrophils and NPP. Neutrophils, activated macrophages and spirochetes as well as other gram-negative bacteria were also prominent in the PATS stained samples. In replicate subgingival plaque smears stained with our procedure for granulocyte peroxidases only neutrophils, budding neutrophils or NPP were readily observed (Fig. 6).

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 NLRP3 Inflammasome Expression in Gingival Crevicular Fluid of Patients with Periodontitis and Chronic Hepatitis C

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Petra Surlin ◽  
Luminita Lazar ◽  
Cerasella Sincar ◽  
Dorin Nicolae Gheorghe ◽  
Dora Maria Popescu ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Periodontal Disease ◽  
Chronic Hepatitis C ◽  
Inflammatory Reaction ◽  
Nlrp3 Inflammasome ◽  
Gingival Crevicular Fluid ◽  
Periodontal Status ◽  
Local Inflammatory Reaction ◽  
Crevicular Fluid

The study is aimed at assessing the impact that periodontal disease and chronic hepatitis C could have on gingival crevicular fluid levels of the NLRP3 inflammasome, caspase-1 (CASP-1), and interleukin-18 (IL-18) and at evaluating whether the increased local inflammatory reaction with clinical periodontal consequences is correlated to their upregulation. Patients were divided into four groups, according to their periodontal status and previously diagnosed hepatitis C, as follows: (i) CHC group, chronic hepatitis C patients; (ii) P group, periodontal disease patients, systemically healthy; (iii) CHC + P group, patients suffering from both conditions; and (iv) H group, systemically and periodontally healthy controls. Gingival crevicular samples were collected for quantitative analysis of the NLRP3 inflammasome, CASP-1, and IL-18. CHC + P patients expressed the worse periodontal status and the highest NLRP3, CASP-1, and IL-18 levels, the difference being statistically significant ( p < 0.05 ). The P group patients also expressed significantly more elevated NLRP3, CASP-1, and IL-18 levels, as compared to nonperiodontal patients (CHC and H groups). Chronic hepatitis C and periodontal disease could have a significant influence on the upregulation of NLRP3 inflammasome and its components, possibly contributing to an increased local inflammatory reaction and clinical periodontal consequences.

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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