Analysis of Gingival Crevicular Fluid as Applied to the Diagnosis of Oral and Systemic Diseases

2007 ◽  
Vol 1098 (1) ◽  
pp. 216-229 ◽  
Author(s):  
I. B LAMSTER ◽  
J. K AHLO
2017 ◽  
Vol 11 (03) ◽  
pp. 407-410 ◽  
Author(s):  
Mojtaba Bayani ◽  
Mohammad Pourali ◽  
Mohammad Keivan

ABSTRACTGingivitis and periodontitis are common bacterial infections caused by a variety of microorganisms. Despite the microorganisms' roles as etiologic agents, inflammation-induced substances also have crucial parts in the loss of connective tissue and the supporting alveolar bone. Visfatin is a pleiotropic mediator, which acts as growth factor, cytokine, and pre-B-cell colony-enhancing factor. A positive correlation was detected between the serum/plasma levels of visfatin and inflammatory disorders such as diabetes mellitus and cardiovascular disease. In addition, the visfatin level was higher in saliva and the gingival crevicular fluid (GCF) of subjects with periodontal disease. This review defined current, predictable patterns of possible interaction of visfatin with periodontal infection and other systemic diseases, using PubMed and Medline databases searching for articles written in English. Peer-reviewed articles were targeted using the following keywords: “visfatin,” “periodontal disease,” “inflammatory mediator,” and “biomarker.” Available full-text articles were read, and related articles were also scrutinized, while a hand search was also performed. Search was confined to human studies, and articles written in English and published between 1985 and 2016 were selected. It was concluded that periodontal infection and other systemic diseases could be related to the levels of visfatin in GCF, saliva, and serum as a biomarker of these diseases.


2009 ◽  
Vol 137 (5-6) ◽  
pp. 298-303 ◽  
Author(s):  
Sasa Cakic

Gingival crevicular fluid (GCF) can be found in the physiologic space (gingival sulcus), as well as in the pathological space (gingival pocket or periodontal pocket) between the gums and teeth. In the first case it is a transudate, in the second an exudate. The constituents of GCF originate from serum, gingival tissues, and from both bacterial and host response cells present in the aforementioned spaces and the surrounding tissues. The collection and analysis of GCF are the noninvasive methods for the evaluation of host response in periodontal disease. These analyses mainly focus on inflammatory markers, such as prostaglandin E2, neutrophil elastase and ?-glucuronidase, and on the marker of cellular necrosis - aspartat aminotransferase. Further, the analysis of inflammatory markers in the GCF may assist in defining how certain systemic diseases (e.g., diabetes mellitus) can modify periodontal disease, and how peridontal disease can influence certain systemic disorders (atherosclerosis, preterm delivery, diabetes mellitus and some chronic respiratory diseases). Major factors which influence the results obtained from the analyses of GCF are not only the methods of these analyses, but the method of GCF collection as well. As saliva collection is less technique-sensitive than GCF collection, some constituents of saliva which originate from the GCF can be analyzed as more amenable to chairside utilization.


2021 ◽  
Author(s):  
Yong Liu ◽  
Renping Zhao ◽  
Bashar Reda ◽  
Wenjuan Yang ◽  
Matthias Hannig ◽  
...  

AbstractIn saliva and gingival crevicular fluid (GCF) soluble factors such as cytokines, chemokines and growth factors have shown a great potential serving as biomarkers for early detection and/or diagnosis of oral and systemic diseases. However, GCF and saliva, which one is a better source is still under debate. This study aimed to gain an overview of cytokines, chemokines and growth factors in saliva and GCF to pave the way for selecting suitable oral fluids for oral and systemic diseases. Multiplex cytokine assay was conducted to determine concentrations of cytokines, chemokines and growth factors in saliva and GCF samples from healthy subjects. The protocol for sample collection was carefully optimized. Stabilization, repeatability, and donor variation of the profiles were analyzed. We found that for different donors, cytokine and chemokine profiles showed unique patterns in saliva but similar patterns in GCF. In terms of growth factors, the profiles were individualized in saliva and GCF. All profiles stayed stable for the same healthy individual. In saliva, profiles of cytokines, chemokines and growth factors are individualized for different donors. In GCF, profiles of cytokines and chemokines are similar. Other factors, such as growth factors and T helper-related cytokines, are highly variable in donors. Profiles of soluble factors are not correlated in saliva and GCF. The comprehensive cytokine profiles in saliva and GCF reported in this work would serve as a good base for choosing promising cytokines for developing biomarkers in oral fluids.


Author(s):  
J Hanker ◽  
E.J. Burkes ◽  
G. Greco ◽  
R. Scruggs ◽  
B. Giammara

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).


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