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)

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

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

Experimental gingivitis provides a useful model for studying the initiation of periodontal disease in man. This study evaluated over a 4-week period the Plaque Index (PLI), Gingival Bleeding Time Index (GBTI), and gingival crevicular fluid (GCF) for resting and flow volume as well as the concentration and total activity of three enzymes in the GCF (lactate dehydrogenase--LDH, beta-glucuronidase--BG and arylsulfatase--AS) from the maxillary right quadrant of eight subjects with healthy gingiva. After rising sharply during the 1st week, the PLI continued to increase during the 2nd week but remained constant during the 3rd and 4th weeks. The GBTI, and the resting and flow GCF volumes, increased steadily throughout the study. LDH concentration in GCF varied minimally during the experiment, while total LDH activity rose slightly over the 4-week period. BG concentration and total activity in GCF rose steadily from baseline to the 3rd week and then either fell or leveled off during the 4th week. AS concentration in GCF rose from baseline to the 2nd or 3rd week and then fell. AS total activity in GCF rose from baseline to the 2nd week and then remained constant. These data suggest that while clinical signs of inflammation increased over the 4 weeks of the experiment, a homeostatic mechanism in the crevicular environment may control ground substance-degrading enzyme activity during experimental gingivitis in man.
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PMID:Lactate dehydrogenase, beta-glucuronidase and arylsulfatase activity in gingival crevicular fluid associated with experimental gingivitis in man. 388 71

In order to simultaneously assess the local humoral immune and polymorphonuclear leukocyte (PMN) responses in periodontal disease, IgG, IgM, and IgA, as well as the PMN lysosomal enzyme beta-glucuronidase (beta G), were examined in gingival crevicular fluid (GCF) from patients with varying degrees of periodontal pathology. Evaluations were made before and after conservative therapy (scaling and root planing). Thirty patients with varying degrees of periodontal pathology, ranging from mild inflammatory gingivitis to moderate periodontitis, were studied. GCF was collected from the mesial surfaces of all teeth. The presence of the 3 immunoglobulin isotypes was determined by enzyme linked immunosorbent assays (ELISA), while total beta G activity in GCF was determined by a fluorometric assay. Clinical parameters were obtained from 6 sites per tooth. Our data indicate that prior to treatment, total beta G activity is strongly related to the severity of periodontal disease as measured by mean probing attachment level (AL; r = 0.89; P < .005), mean probing depth (PD; 4 = 0.89; P < .0005) and percentage of sites exhibiting bleeding on probing (% BOP; r = 0.49; P < .005). Following treatment, no statistically significant relationship of disease severity and beta G is found. The concentrations of IgG and IgM in GCF do not follow a specific pattern when related to disease severity. In contrast, prior to treatment the concentration of IgA is negatively correlated to mean AL (r = -0.54; P < .005), mean PD (r = -0.59; P < .005), and % BOP (r = -0.47, P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoglobulin isotypes in gingival crevicular fluid: possible protective role of IgA. 789 Dec 51

Previous reports have suggested that persistently elevated levels of the acidic glycohydrolase beta-glucuronidase (beta G) in gingival crevicular fluid (GCF) can identify patients with chronic adult periodontitis who are at risk for future probing attachment loss (PAL). To comprehensively study beta G activity in GCF, a multicenter trial examining the relationship of the enzyme in GCF to traditional clinical parameters of periodontal disease and PAL was conducted. In this report, the baseline data was used to evaluate the relationship of beta G activity in GCF to traditional parameters of periodontal disease. The study group included 130 patients who had been treated for periodontal disease and were on a regular recall schedule, and 10 patients with chronic adult periodontitis who had never received treatment. Upon entering the longitudinal trial, the patients were examined, and a standardized 30-s GCF sample was collected from the mesiobuccal crevice of all study teeth. As a control, GCF samples and clinical data were collected from 62 patients with a healthy periodontium or mild inflammatory gingivitis without loss of probing attachment. At baseline, beta G activity for the periodontitis patients ranged from 0 to 1704 Units (U), with a median of 32 U. beta G could not be detected in 0.2% of samples (activity < or = 2.0 U). The 90% cumulative relative frequency was 139 U. For the healthy/gingivitis subjects beta G activity ranged from 0 to 504 U, with a median of 22 U. Enzyme was not detectable in 0.4% of samples. Only 0.9% of samples contained greater than 139 U. beta G activity in GCF was not related to gender or age. For the periodontitis patients, elevated enzyme activity (> or = 140 U) was most often associated with molar teeth, followed by maxillary bicuspids. Maxillary central incisors, and mandibular central and lateral incisors displayed the lowest frequency of elevated enzyme activity. The relationship of beta G activity to the traditional parameters of probing depth and bleeding on probing was assessed. For shallow sites (1.0-1.5 mm, 2.0-2.5 mm probing depth), the large majority of GCF samples contained low enzyme activity (90% of samples < 50 U). Descriptive indicators demonstrated a trend of increased beta G activity with increased probing depth. The median beta G activity shifted from 15 U for the shallowest sites (1.0-1.5 mm) to 127 U for the deepest sites (5-8 mm). However, this was due to a broadening of the distribution rather than representing a shift in the distribution profile.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The relationship of beta-glucuronidase activity in crevicular fluid to clinical parameters of periodontal disease. Findings from a multicenter study. 814 31

Several neutrophil-derived enzymes that are present in the gingival crevicular fluid have been evaluated for use as risk markers for periodontal disease progression. However, very little information is available about the presence of these enzymes in peri-implant tissues. The purpose of this cross-sectional study was to compare levels of enzymes in gingival crevicular fluid between natural teeth and endosseous dental implants and between well-integrated and failing implants. Scores of plaque and gingivitis were recorded for 68 integrated implants, five failing implants, and 34 natural teeth in 12 completely edentulous and 18 partially edentulous subjects. Samples of gingival crevicular fluid were obtained from these sites using filter paper strips and were assayed for levels of neutral protease, neutrophil elastase, myeloperoxidase, and beta-glucuronidase. Neutral protease levels were higher (P = .066) at moderately to severely inflamed implant sites (Gingival Index of 2, 3) compared to mildly or noninflamed sites (Gingival Index of = 0, 1). Despite the small number (n = 5) of failing implants evaluated in this study, levels of neutrophil elastase, myeloperoxidase, and beta-glucuronidase were significantly higher (P < or = .001) around failing implants compared to successful implants. Neutral protease levels were also elevated around failing implants, but the difference was not statistically significant. Results of this study indicate that neutrophil elastase, myeloperoxidase, and beta-glucuronidase levels in GCF appear to be good candidates for study as risk markers of implant failure.
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PMID:Crevicular fluid enzymes from endosseous dental implants and natural teeth. 875 53

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

A review of periodontal disease as a manifestation of HIV infection suggests a shift in emphasis over the past 5 years. Initially the focus was on newly described forms of periodontal disease (i.e., HIV-associated gingivitis or linear gingival erythema (LGE); HIV-associated periodontitis or necrotizing ulcerative periodontitis (NUP). While the clinical definition of LGE varies from study to study, an association between LGE and Candida infection has been described. Furthermore, the prevalence of NUP is quite low and this disorder is associated with severe immunosuppression. In contrast, the focus today is on the accelerated rate of chronic adult periodontitis occurring in seropositive patients. While the organisms that characterize adult periodontitis in seronegative individuals are present in subgingival plaque from seropositive individuals, reports suggest that atypical pathogens are also present (i.e., Mycoplasma salivarium, Enterobacter cloacae). Recent studies from our laboratory have identified a novel strain of Clostridium isolated from the subgingival plaque of injecting drug users that has pathologic potential. This organism, however, was found in both seropositive and seronegative individuals in this cohort, suggesting an association with lifestyle rather than serostatus. In addition, data has been published examining the local host response in periodontitis in seropositive individuals. Distinctly elevated levels of IgG in gingival crevicular fluid (GCF) have been observed in seropositive patients. Furthermore, data from our laboratory examining inflammatory mediators in GCF (polymorphonuclear leukocyte lysosomal enzyme beta-glucuronidase and the pro-inflammatory cytokine interleukin-1 beta) suggests an altered response in patients with HIV infection. The alteration manifests as the absence of the expected strong correlation between polymorphonuclear leukocyte activity in the gingival crevice and clinical measures of existing periodontal disease, as well as elevated levels of interleukin-1 beta in sites with deeper probing depths. Therefore, it can be concluded that the progression of periodontal disease in the presence of HIV infection is dependent upon the immunologic competency of the host as well as the local inflammatory response to typical and atypical subgingival microorganisms.
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PMID:Epidemiology and diagnosis of HIV-associated periodontal diseases. 945 78

Periodontal manifestations of human immunodeficiency virus (HIV) infection were first described in 1987. Initially, the lesions receiving attention were HIV-associated gingivitis (now known as linear gingival erythema [LGE]) and HIV-associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (< or = 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV- patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV- injecting drug users (IDU), levels of the proinflammatory cytokine interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (> or = 4 mm), total IL-1 beta in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase beta-glucuronidase (beta G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total beta G in GCF and probing depth in the HIV-IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total beta G was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute total periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss.
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PMID:New concepts regarding the pathogenesis of periodontal disease in HIV infection. 972 91


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