Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cross-sectional study of 117 subjects from a dental clinic serving a diverse population (i.e., Whites, African-Americans, Native-Americans, and Asians) was performed to evaluate risk indicators of periodontal disease. Gingival crevicular fluid (GCF) and subgingival plaque were taken at the same visit from 4 posterior sites of the most diseased sextant in each subject. Age, smoking packyears, beta-glucuronidase (beta G), neutrophil elastase (NE), myeloperoxidase (MPO), Fusobacterium nucleatum (F. nucleatum), and Porphyromonas gingivalis (P. gingivalis) were significantly (p < 0.05-0.005) correlated with attachment loss. Probing depth was significantly correlated with smoking packyears, beta G, NE, MPO, F. nucleatum and Prevotella intermedia (P. intermedia) (p < 0.05-0.005). Mean NE value of Whites was lower than the mean NE values of African-Americans, Native-Americans and Asians (p < 0.05). Whites had a lower mean beta G value compared to African Americans, and a lower mean MPO value compared to African Americans and Native Americans. The %s of patients positive for F. nucleatum, P. intermedia and Eikenella corrodens (E. corrodens) were higher in Native Americans compared to Whites. Step-wise multiple regression analysis was performed to construct models for the estimation of probing depth and attachment loss. The most parsimonious regression models which had the best R2 values included the following variables and accounted for the indicated % of variability: models 1 and 2: beta G, race, and F. nucleatum accounted for 50% of the variability in mean probing depth and 39% of the variability in a single site (first molar) for probing depth, respectively; model 3: age, beta G, and F. nucleatum accounted for 53% of the variability in mean attachment loss; model 4: age, NE, and F. nucleatum explained 35% of the variability in a single site (first molar) for attachment loss. The results suggest that age, race, smoking packyears, beta G, NE, MPO, F. nucleatum, P. gingivalis and P. intermedia are risk indicators for periodontal disease in this racially diverse urban population. Regression models which include multiple variables (i.e., demographic factors, GCF enzymes and periodontopathic bacteria) can be used to estimate periodontal disease status.
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PMID:Risk indicators for periodontal disease in a racially diverse urban population. 895 24

Gingival crevicular fluid (GCF) is an inflammatory exudate that can be collected at the gingival margin or within the gingival crevice. The biochemical analysis of the fluid offers a noninvasive means of assessing the host response in periodontal disease. In recent years, the relationship of measures of the inflammatory response in GCF to risk for development of active periodontal disease (defined as clinical attachment loss or radiographic bone loss) has been studied in longitudinal trials. The greatest interest has focused on prostaglandin E2, an arachidonic acid metabolite; beta-glucuronidase and neutrophil elastase, markers of lysosomal enzyme release from neutrophils; and aspartate aminotransferase, a cytoplasmic enzyme indicative of cellular necrosis. Analysis of the data allows a number of conclusions to be drawn concerning the potential diagnostic significance of GCF: 1) an exuberant host inflammatory response is associated with progressive disease in patients with periodontitis; 2) collection of GCF using small precut strips is a reproducible and reliable collection technique; 3) the total amount of the mediator and not concentration of the mediator in the GCF sample can be reported when timed samples are collected; and 4) technology exists for GCF-based diagnostic tests to be performed in the dental office. Nevertheless, many questions remain. Still to be determined are: 1) the relationship of test results to the development of periodontitis in patients with gingivitis; 2) the level of test accuracy needed to justify use of these tests; 3) the unit of observation (patient, site) that is being evaluated by the test; and 4) the need for such tests as perceived by clinicians. While these questions are formidable, introduction of GCF-based diagnostic tests will provide clinicians with an improved, quantitative means of evaluating patients and offer specific criteria to assess the effectiveness of treatment.
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PMID:Evaluation of components of gingival crevicular fluid as diagnostic tests. 915 49

There have been no reports on the relationship of subgingival temperature to specific gingival crevicular fluid (GCF) components. Therefore, the purpose of this cross-sectional study was to determine whether there was any relationship between subgingival temperature and GCF levels of neutrophil elastase (NE), myeloperoxidase (MPO), beta-glucuronidase (BG), interleukin-1 alpha (IL-1), and interferon alpha (IFN). Furthermore, another objective was to confirm an association of subgingival temperature with clinical parameters and specific subgingival plaque micro-organisms as has been reported earlier. 27 human subjects each having healthy (n = 50), gingivitis (n = 59) and periodontitis (n = 53) sites were evaluated. The plaque index (PI), subgingival temperature, probing depth, attachment loss, bleeding index and gingival index were measured. GCF was sampled following the measurement of the PI and removal of the supragingival plaque. GCF samples were assayed for the enzymes NE, BG, MPO and the cytokines IFN-alpha and IL-1 alpha. A sterile Gracey curette was utilized at each sampled site to collect subgingival plaque. The plaque samples were evaluated using an immunoassay. Subgingival temperature was found to directly correlate with all clinical parameters (p < 0.001). Significant, albeit not large, correlations were found between subgingival temperature and NE (r = 0.35, p < 0.001), MPO (r = 0.26, p < 0.001) and BG (r = 0.23, p < 0.01). Temperature was found to correlate positively with E. corrodens (r = 0.33, p < 0.02) and F. nucleatum (r = 0.25, p < 0.05) but not with P. intermedia (r = 0.02, p = 0.9), P. gingivalis (r = 0.20, p = 0.1) and A. actinomycetemcomitans (r = 0.01, p > 0.9). In conclusion, subgingival temperature is correlated with the GCF enzymes, NE, MPO and BG as well as the clinical parameters and specific plaque micro-organisms associated with periodontal disease.
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PMID:Subgingival temperature: relation to gingival crevicular fluid enzymes, cytokines, and subgingival plaque micro-organisms. 944 27

Circulating human neutrophils from patients with severe inflammatory disorders such as erysipelas and sepsis are specifically desensitized to complement factor C5a stimulation but not to stimulation with other stimuli like N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-8 (IL-8), leukotriene B4 (LTB4), or platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). In this study, we raised the question whether factors released from polymorphonuclear leukocytes (PMNs) can specifically down-regulate C5a-dependent neutrophil functions. When neutrophils were preincubated with either neutrophil lysates or neutrophil degranulation supernatants, a complete inhibition of C5a-stimulated beta-glucuronidase release and chemotaxis could be observed, whereas FMLP-, IL-8-, LTB4- or PAF-dependent functions were not affected. Serine protease inhibitors like phenylmethylsulfonyl fluoride, antileukoprotease, or elafin abolished this effect. High-performance liquid chromatography of neutrophil degranulation supernatants revealed pronounced inhibition of C5a-dependent neutrophil functions in fractions exerting elastase or cathepsin G activity, but not in fractions exerting proteinase 3 activity. Using purified human leukocyte elastase (HLE), C5a responses like intracellular calcium influx, beta-glucuronidase release, and chemotaxis were also specifically inhibited. Our experiments show that the release of HLE or cathepsin G from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a. Elastase and cathepsin G may therefore play an important role in the down-regulation of acute inflammation.
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PMID:Human leukocyte elastase and cathepsin G are specific inhibitors of C5a-dependent neutrophil enzyme release and chemotaxis. 1514 22

Gingival crevicular fluid (GCF), a serum transudate or inflammatory exudate, can be collected from the gingival crevice surrounding the teeth. As such, the fluid reflects the constituents of serum, the cellular response in the periodontium, and contributions from the gingival crevice. The study of GCF has focused on defining the pathophysiology of periodontal disease, and identification of a potential diagnostic test for active periodontitis. The majority of markers that have been identified as potential candidates for such a test are measures of inflammation (i.e., prostaglandin E2 (PGE2), neutrophil elastase, and the lysosomal enzyme beta-glucuronidase). Further, analysis of inflammatory markers in GCF may assist in defining how certain systemic disorders (e.g., diabetes mellitus) can modify periodontal disease, and how periodontal disease/periodontal inflammation can influence certain systemic disorders (i.e., cardiovascular/cerebrovascular diseases). Methodological concerns related to the collection and analysis of GCF are important factors that need to be considered when studying GCF. Practical concerns argue against the widespread clinical application of GCF as an adjunct to periodontal diagnosis. Rather, analysis of GCF-derived mediators in saliva may serve as a means of rapid screening for periodontal disease.
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PMID:Analysis of gingival crevicular fluid as applied to the diagnosis of oral and systemic diseases. 1743 31

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 beta-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 analysed as more amenable to chairside utilization.
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PMID:[Gingival crevicular fluid in the diagnosis of periodontal and systemic diseases]. 1959 76


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