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)

Five enzymes have been studied to differentiate between T and B lymphocytes in sections of human lymph nodes, tonsils and chronic inflammatory periodontal disease. The presence of acid phosphatase, beta-glucuronidase N-acetyl-beta-glucosaminidase, non-specific esterase and fluoride-resistant esterase activity was determined histochemically. The results indicate that cells in the B area of both lymph nodes and tonsils are negative for enzyme activity, while those in the T area show a single intense granule of activity. These enzymes were unable to differentiate between T blasts, B blasts and plasma cells in the sections studied. The majority of the lymphoid cells in the lesions of chronic inflammatory periodontal disease are enzyme-negative and probably of B-cell origin.
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PMID:Enzyme differentiation of lymphocyte subpopulations in sections of human lymph nodes, tonsils and periodontal disease. 30 63

Traditional clinical variables of periodontal pathology have only limited value as indicators for future disease progression in patients with adult periodontitis. Consequently, other aspects of the periodontal lesion are being examined for their diagnostic utility. Analysis of the host response in gingival crevicular fluid (GCF) is among the most intensely studied of these new diagnostic approaches. Specific indicators of the humoral immune response, cellular immune response, and acute inflammatory response have been identified in GCF. The relationship of indicators of the humoral immune response to active periodontal disease is equivocal. Specific indicators of the cellular immune response in GCF may ultimately prove to be important diagnostically, but the relationship of any specific marker to active periodontal disease has not been reported. In contrast, the acute inflammatory response in GCF has been extensively studied and a number of factors appear to be associated with an increased risk for future disease progression. Indicators of enhanced polymorphonuclear leukocyte activity, (lysosomal beta-glucuronidase, lysosomal collagenase), prostaglandin E2, and an indicator of acute tissue destruction (the cytoplasmic enzymes aspartate aminotransferase) have been associated with the occurrence of clinical attachment loss. An example of the application of a GCF marker in a periodontitis clinical trial is provided by describing the relationship of lysosomal beta-glucuronidase in GCF at baseline and 2 weeks following root planing and scaling to the occurrence of disease activity during the following 6 months. Persistently elevated levels of this enzyme were related to clinical attachment loss. The positive, negative, and total predictive values for beta-glucuronidase as an identifier of clinical attachment loss were 86%, 71%, and 76%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The host response in gingival crevicular fluid: potential applications in periodontitis clinical trials. 147 31

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 beta-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-1 alpha, IL-1 beta, tumor necrosis factor-alpha), 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-1 beta and TNF-alpha, 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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PMID:Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 173 70

In the present review, the composition of the gingival crevicular fluid (GCF) as well as its important role in the diagnosis of periodontal disease have been discussed. Furthermore, the different sampling methods and the subsequent analytical procedures have been described. Some of the GCF-components, such as elastase, prostaglandin, arylsulphatase and beta-glucuronidase, are examined for their use as suitable markers of future disease activity. At the present time, the interest of research is focussing on the host-parasite interaction, the prediction of disease activity, and the identification of risk groups of patients. Therefore, GCF is considered a valuable research subject and a possible diagnostic marker.
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PMID:[Sulcus fluid in periodontal diagnosis. A review]. 188 20

Two test teeth, anteriors with greater than or equal to 6 mm deep periodontal pockets from each of 10 patients with advancing periodontitis were included in this study. The clinical signs of advancing periodontitis, generalized moderate to deep pockets and to severe loss of alveolar bone, were observed in young adult. There have been several reports on factors, which reflect the conversion clinically from infection by highly pathogenic plaque bacteria to a from of periodontitis displaying relatively rapid loss of clinical attachment. The purpose of this investigation was to detect parameters in fluid, which could leak from the underlying inflamed connective tissue into the gingival crevice, and which could shown correlatively the progressive variations of periodontal disease by recurrent acute stage. In order to determine active disease sites and to monitor guantitatively response to therapy or to measure degree to susceptibility of future breakdown. Examinations on following parameters at pre- and post- periodontal treatment stages were carried out. Endotoxin, collagenase, alkaline phosphatase, beta-glucuronidase, interleukin-1 alpha, IgG antibody levels to Bacteroides gingivalis, Bacteroides intermedius were measured in gingival exudate samples, which were collected by the microtips technique from periodontal pockets. The following results were obtained: 1) Considering the effect of periodontal therapy, pathogenic responses on total colony forming unit (CFU), interleukin-1 alpha and changes of endotoxin and beta-glucuronidase levels after the treatment have indicated that specific changes in humoral responses. 2) There was not significant relation between alkaline phosphatase, collagenase, IgG antibodies level to Bacteroides gingivalis, Bacteroides intermedius and responses in active and also inactive disease sites. 3) This study has been resulted in the development of diagnostic techniques which requires strict criteria on the disease activity of the periodontal disease very specific in order to permit a more scientific approach to the care of periodontitis patients and to speculate the prognosis of the patients after the treatment.
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PMID:[Changes of factors on disease activity in advancing periodontitis]. 213 9

The tissue destruction resulting from release of lysosomal enzymes by exocytosis and degranulation of polymorphonuclear leucocytes in host gingiva may contribute significantly to periodontal diseases. In this investigation peripheral blood was obtained from healthy controls and otherwise healthy individuals with rapidly progressive periodontitis. Polymorphonuclear leucocytes were isolated and suspended in HBSS for subsequent in vitro FMLP challenge to induce degranulation. The supernatant was tested for beta-glucuronidase. Polymorphonuclear leucocytes from patients with rapidly progressive periodontitis contained significantly higher absolute amounts of beta-glucuronidase (p less than 0.001) and released greater amounts at various molarities of FMLP antigenic challenge (p less than 0.01). Such an increase in lysosomal enzyme activity may provide an enhanced potential for tissue destruction in this periodontal disease.
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PMID:Increased intracellular levels of beta-glucuronidase in polymorphonuclear leucocytes from humans with rapidly progressive periodontitis. 237 86

The potential application of gingival crevicular fluid (GCF) analysis to periodontal diagnosis has been examined for more than 25 years. Unfortunately, the information available has not provided the clinician with a more sensitive means of diagnosing periodontal disease or an effective means of monitoring periodontal therapy. A careful review of the literature on GCF, however, suggests that discrepancies occur in the method of GCF collection, the use of GCF for analysis from pooled or isolated crevicular locations, the method of analyzing the samples and the way in which the data is reported. Studies in our laboratory have suggested a technique for GCF analysis that collects GCF from individual crevices with a filter paper strip inserted for a standard time, determines the volume of GCF collected with a calibrated electronic meter and elutes the material into a larger volume of diluent. This approach allows for detection of site-to-site and patient-to-patient differences in GCF volume while providing sufficient samples to analyze GCF for multiple constituents. We have used this approach to evaluate GCF for vertebrate forms of the enzymes collagenase (latent and active forms), beta-glucuronidase and arylsulfatase during the development of experimental gingivitis in man. Interproximal and midradicular areas were studied. Our results indicate that during the 4 weeks of the gingivitis, the absolute amount of active collagenase in GCF increased 550% at the interproximal sites and 190% in the midradicular sites, and the per cent of active collagenase increased from 15 to 71% at the interproximal sites, and from 16 to 36% at the midradicular sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of a biochemical profile for gingival crevicular fluid. Methodological considerations and evaluation of collagen-degrading and ground substance-degrading enzyme activity during experimental gingivitis. 300 Dec 65

A case of infantile agranulocytosis with survival into adolescence is presented. The polymorphonuclear leukocyte is considered an important source of lysosomal enzymes in gingival crevicular fluid, and evaluation of connective tissue-degrading enzymes in the fluid was performed. The activity of beta-glucuronidase, a ground substance-degrading enzyme that may serve as a marker for polymorphonuclear leukocytes, was markedly reduced in the fluid compared to samples from systemically healthy adults with periodontitis. The activities of the ground substance-degrading enzyme arylsulfatase, and collagenase, were in the low-normal range. The plaque microbiology, as characterized by dark-field microscopy and selective culturing, was consistent with advanced periodontitis. A review of the medical history revealed a series of bacterial infections since infancy. Improvement in the systemic health of the patient occurred at about the age of 15, and the intake of antibiotics to control infections was correspondingly reduced after this time. An exacerbation of the patient's periodontal disease, as evaluated by loss of alveolar bone on radiographs, occurred 1 to 2 years later. The progression of periodontal disease observed in this patient was apparently associated with the withdrawal of antibiotics administered for control of systemic (nonoral) infections.
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PMID:Infantile agranulocytosis with survival into adolescence: periodontal manifestations and laboratory findings. A case report. 302 96

Chronic inflammatory processes are often associated with bone resorption. Stimulated by the current great interest in the role of coagulation factors in inflammation and immune injury, we have studied the effect of thrombin on mouse calvarial bones in vitro. Thrombin caused a dose-dependent (0.1-7 U/ml) stimulation of 45Ca release from neonatal mouse calvarial bones. Thrombin also stimulated the mobilization of stable calcium and inorganic phosphate, the release of 3H from [3H]proline-labelled calvaria, the production of lactate and the release of the lysosomal enzymes, beta-glucuronidase and beta-N-acetylglucosaminidase. Thrombin also enhanced 45Ca release from fetal rat long bones, although this bone resorption assay was less sensitive to thrombin than the mouse calvarial system. The bone resorption stimulatory activity of thrombin in mouse calvaria could be inhibited by calcitonin and an increased concentration of phosphate in the culture medium. Thrombin-induced 45Ca release in mouse calvaria was sensitive to inhibition by hydrocortisone and dexamethasone. By contrast, 45Ca release response to parathyroid hormone was insensitive to corticosteroids. The prostaglandin synthetase inhibitors indomethacin, meclofenamic acid and naproxen and 5,8,11,14-eicosatetraynoic acid reduced 45Ca release from thrombin-stimulated calvaria. However, significant stimulation by thrombin could be achieved also in bones treated with inhibitors of arachidonate metabolism. The results obtained suggest that thrombin can stimulate cell-mediated bone resorption by an osteoclast-dependent mechanism. The mechanism of action may involve both prostaglandin-dependent and prostaglandin-independent pathways. Our findings indicate that thrombin may contribute to the bone resorptive processes seen in periodontal disease and rheumatoid arthritis.
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PMID:Blood coagulation and bone metabolism: some characteristics of the bone resorptive effect of thrombin in mouse calvarial bones in vitro. 312 18

The biochemical analysis of gingival crevicular fluid (GCF) may offer a sensitive means of determining periodontal disease activity, including the transition of gingivitis to periodontitis. To continue our evaluation of the relationship between clinical and GCF parameters, 552 sites with shallow to intermediate (2.0-5.0 mm) probing depths (PD) were examined. The data were collected at baseline from 33 periodontitis patients participating in a longitudinal trial examining the relationship of changes in GCF biochemistry to attachment loss. Mesiobuccal sites were scored for dichotomous measures of bleeding on probing, gingival redness, suppuration, and plaque accumulation. In addition, GCF was collected using filter paper strips inserted into the sulcus for 30 seconds, eluted in buffer and assayed for activity of the enzymes beta-glucuronidase (BG), arylsulfatase (AS), and lactate dehydrogenase (LDH), markers for ground substance-degradation and cellular necrosis, respectively. Clinical and GCF parameters were evaluated by increasing PD. Plaque accumulation and bleeding on probing increased with increasing PD, although there was considerable overlap across groups. Suppuration was present in only a very small number of sites and the proportion of sites displaying gingival redness was not related to PD. GCF volume was grouped in 0.25-microliter increments, revealing a progressive shift with increasing PD toward a normal distribution around the median range of 0.51 to 0.75 microliter at 5.0 mm. Mean enzyme activities of BG, and to a lesser extent AS and LDH increased sharply from 2.0 to 3.0 mm, were relatively stable from 3.5 to 4.5 mm, and were significantly higher in 5.0 mm than 4.5 mm sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lysosomal and cytoplasmic enzyme activity, crevicular fluid volume, and clinical parameters characterizing gingival sites with shallow to intermediate probing depths. 330 52


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