Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gingival crevicular fluid samples were collected from 296 teeth from 40 subjects, including 19 rapidly progressive periodontitis (RPP), 8 chronic adult periodontitis (CAP), 7 marginal gingivitis (MG) and 6 healthy subjects (H). The activities of aspartate aminotransferase (AST) in each sample were tested. The results were as follows: (1) The two groups with destructive periodontal disease (RPP and CAP) had greater GCF-AST levels than that from the two non-destructive groups (MG and H). (2) The GCF-AST activities showed significant positive correlations with clinical periodontal parameters, such as probing depth, attachment loss, bleeding index and suppuration. (3) Four weeks after thorough full-mouth root planing, both clinical parameters and GCF-AST levels decreased significantly. The present study suggests that GCF-AST activity might be a sensitive and objective marker for detection of periodontal tissue destruction and inflammation.
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PMID:[Gingival crevicular aspartate aminotransferase levels in periodontitis patients before and after periodontal treatment]. 128 91

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

Extensive data collected over the past decade demonstrate clearly that disease-active and disease-inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease-active and disease-inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline phosphatase, beta-glucuronidase, prostaglandin-E2, aspartate aminotransferase, and IgG4 antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on beta-glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with early-onset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE2 and Interleukin-1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site-specific disease activity. However, the capacity of an individual to mount an IgG2 subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility.
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PMID:Host response tests for diagnosing periodontal diseases. 157 49

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

During a 2-year period pocket depth, probing attachment level, gingival index, and crevicular fluid aspartate aminotransferase (AST) levels were monitored in 25 previously treated periodontitis patients. Probing attachment level change was used retrospectively to identify sites where active periodontal destruction had occurred. The ability of crevicular fluid AST activities at 600, 800, 1000, and 1200 microIU levels to recognize active disease was investigated. Probing attachment level changes observed support the concept that the pattern of periodontal disease activity is episodic and infrequent. A loss of greater than or equal to 2 mm was found at 11% of all studied sites, whereas a gain of greater than or equal to 2 mm was noticed for 15% of sites. 2 subjects had 3 teeth that lost greater than or equal to 2 mm of attachment, whereas 15 subjects demonstrated no teeth with disease activity. The remaining 8 subjects had 1 or 2 sites that lost greater than or equal to 2 mm of attachment. Bayes's theorem and ROC curves were used to exemplify the sensitivity and the specificity of AST assessments. The AST 800 microIU demonstrated a sensitivity of 0.93 and specificity 0.68 and an odds ratio of 15.4 for attachment loss greater than or equal to 2 mm. Under the conditional probability of either 50%, 25% or 10% active disease prevalence, AST 800 microIU has a predictability of 73%, 50% and 24% respectively.
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PMID:Diagnostic characteristics of crevicular fluid aspartate aminotransferase (AST) levels associated with periodontal disease activity. 173 8

Previous studies have shown that aspartate aminotransferase (AST), an established serum marker for cardiac and liver damage in humans, appears in elevated concentrations in samples of gingival crevicular fluid (GCF) from ligated vs. non-ligated teeth in beagle dogs and in elevated quantities in cross-sectional GCF sampling, adjusted for collection time, from human sites with clinical signs of past or present periodontal disease as compared to healthy sites. This paper describes a longitudinal study in which AST was monitored quarterly over a 2-year period at 2 sites/tooth in 31 patients with mild to moderate adult periodontitis. In this study sample, 40 (2.6%) of 1536 sites exhibited confirmed loss of at least 2 mm of attachment during the 2-yr observation period. In comparison with healthy sites within the same patients, AST standardized to a 30-second collection interval (AST30) was elevated at these sites with new confirmed attachment loss, and at sites with past attachment loss or gingivitis in the absence of periodontitis. When both within- and between-patient variation were taken into account, observed odds-ratios associating enzyme with disease were higher for sites with new attachment loss (9-16 depending on test cut-point) than for sites with pre-study attachment loss (3-12), or gingivitis in the absence of periodontitis (5-8). AST in GCF is strongly related to human periodontal disease. The data are consistent with the hypothesis that the relationship is strongest during episodes of cumulative tissue breakdown, but the small numbers of sites with confirmed attachment loss during the study period, or with gingivitis in the absence of periodontitis, means that further clinical studies are necessary to clarify this issue.
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PMID:A longitudinal study of aspartate aminotransferase in human gingival crevicular fluid. 182 27

Previous investigation has shown that the concentration of aspartate aminotransferase (AST), an established serum marker for cardiac and liver damage in humans, is significantly elevated in samples of gingival crevicular fluid (GCF) from ligated teeth in beagle dogs. This paper reports on a cross-sectional study of the relationships between AST in GCF and clinical indices of human periodontal disease in 60 patients with mild to moderate adult periodontitis. AST standardized to a 30-second collection interval (AST30) showed substantial (multiple regression R2 = 0.61) association with summary indices of patient disease status, modest association (partial R2 = 0.22) with tooth disease status within patient, and weaker (partial R2 = 0.12) but statistically significant association with site-to-site variation in disease at the same tooth. AST concentration showed modest (R2 = 0.30) between-patient relationship with clinical indices, but no clinically significant relationship with these indices between sites within patients, suggesting a rough proportionality between accumulated enzyme and GCF volume at sites with varying stages of disease. The relationship between GCF volume and probing depth also appears central to interpretation of enzyme assays. Clinical measures of past periodontitis and current inflammatory disease are cross-sectionally related to variation in AST30, across patients and sites within the same patient. Considerable residual variation, especially elevated AST30 in the absence of clear signs of disease, may result from varying levels of current disease activity, not reflected in clinical measures.
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PMID:A cross-sectional analysis of aspartate aminotransferase in human gingival crevicular fluid. 182 28

Periodontal diseases and patients at risk for progression of disease can be diagnosed on the basis of age, previous episodes of periodontal disease and loss of attachment, as detected by periodontal probing and radiographic evaluation. For early onset periodontitis, family history may be important. Microbiological evaluations are excellent determinants of disease and also appear to be probable predictors of 'at risk' patients. Reliable tests, including chairside tests, are available for the three most probable pathogens: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia. Biochemical changes, although associated with various disease states, are not yet readily measurable at the chairside, with the exception of one test that measures aspartate aminotransferase and shows promise as a detector and predictor of periodontal disease. The diagnosis and 'at risk' prediction of periodontal disease is based on a number of criteria, some of which are highly reliable and others whose reliability is either probable or unclear. These criteria are reviewed with emphasis on those that may be indicative of the patient at high risk of developing periodontal disease or progressing to a more severe form of disease.
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PMID:Detection and management of the high risk periodontal patient. 193 50

Previous investigations have shown a clear association between the presence of the enzyme aspartate aminotransferase (AST) in gingival crevicular fluid (GCF) and clinical evidence of periodontal disease in humans, as well as in the beagle dog model. This paper describes a 26-week study that uses the beagle dog model of ligature-induced periodontitis in which GCF-AST (corrected for collection time) was correlated with microscopic evidence of tissue destruction in the periodontium at the sites of fluid collection. GCF and clinical data were collected at baseline, at optimal gingival health, during gingivitis, and after ligation. A cross-mouth design was implemented so that six premolar teeth in each dog were ligated for periods up to five weeks. Formalin-fixed tissues from the sites of GCF collection were prepared for light microscopy and evaluated for the presence of epithelial ulceration, bone resorption, and inflammatory cell infiltration. The relationship between GCF-AST levels and microscopic findings was analyzed by calculation of sensitivity and specificity and by plots of Receiver Operating Characteristics. These data revealed a correlation between elevated enzyme concentration and microscopic evidence of disease activity. Taken together with human studies, these results provide support for the use of AST as a marker of periodontal disease progression.
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PMID:Association of gingival crevicular fluid aspartate aminotransferase levels with histopathology during ligature-induced periodontitis in the beagle dog. 204 80

Data from several sources demonstrate that disease-active and disease-inactive periodontal pockets exist, and that disease progression occurs in bursts of activity. Currently used diagnostic procedures do not distinguish between disease-active and disease-inactive sites at any given point in time. We report the results of studies aimed at determining whether levels of the enzyme aspartate aminotransferase (AST) in gingival crevicular fluid (GCF) are associated with disease activity as assessed by the level of gingival inflammation and probing attachment loss. 25 previously treated periodontitis patients participating in a quarterly recall maintenance program, who had experienced recurrent periodontal deterioration, served as experimental subjects. Patients were evaluated at 3-month intervals for 2 years. Values for plaque index, gingival index, and probing attachment level were recorded, and 30-second samples of gingival fluid harvested from the mesiobuccal aspect of the 4 first molars and the distal of the 4 lateral incisors. GCF volume was measured using a Periotron 6000, and AST activity was measured by a standard method. Sites were ranked in a hierarchy based on the degree of certainty of attachment loss as well as the severity of gingival inflammation, and the relationship of the values to AST levels was determined. Three models were used to analyze the resulting data, and all led to the same conclusion. Maximum enzyme level was significantly elevated at sites with confirmed disease activity as assessed by attachment loss, with maximum AST levels 725 units higher at these sites, on average, than at other sites (p less than 0.0001). Our data support the idea that an objective diagnostic test, based on levels of AST in GCF, that distinguishes between disease-active and disease-inactive sites may be possible.
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PMID:Relationship between gingival crevicular fluid levels of aspartate aminotransferase and active tissue destruction in treated chronic periodontitis patients. 213 21


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