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:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been proposed that Bacteroides gingivalis and Actinomyces viscosus are most important agents to pathogenesis of the periodontitis and gingivitis. In this study, the influences of sonic extracts prepared from B. gingivalis and A. viscosus for DNA synthesis of murine lymphocytes, production of prostaglandin E2 (PGE2), collagenase and interleukin-1 (IL-1) from human peripheral monocyte were investigated. Furthermore, PGE2 and collagenase production by fibroblasts from human periodontal ligament (HPLF) and gingiva (Gin 1) stimulated with macrophage conditioned medium (MCM) cultured with bacterial sonic extracts were examined. The results obtained were as follows. 1. The sonic extracts (10 micrograms/ml protein) from B. gingivalis and A. viscosus showd low mitogenic activity to spleen cells, however, induced polyclonal B cell activation. 2. Although, the effect of these sonic extracts on the production of PGE2 and collagenase by human peripheral monocyte was not found, the induction of IL-1 production was recognized. 3. The culture supernatants of C3H/HeN mouse peritoneal macrophage stimulated with sonic extracts of B. gingivalis and A. viscosus were induced PGE2 and collagenase production by HPLF and Gin 1. These results suggest that the cellular components of B. gingivalis and A. viscosus may play the pathogenic roles in periodontal tissue destruction through the stimulation of macrophage and/or lymphocyte.
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PMID:[Studies on immunobiological activities of periodontopathic bacteria. Comparison of the activities of soluble components from Bacteroides gingivalis and Actinomyces viscosus]. 196 95

The present study was performed to investigate the effects of endotoxins from periodontopathic bacteria on collagen metabolism. Endotoxins were extracted from Bacteroides gingivalis 381 and Bacteroides intermedius ATCC 25611 using the hot-phenol method. A commercially available endotoxin from Escherichia coli 0111: B4 was also used as a control. Human gingival fibroblasts (Gin-1, ATCC CRL 1292) were maintained with DMEM containing 10% FBS. When the fibroblasts became confluent they were exposed to each of the endotoxins in various concentrations (0, 5, 10, 15, 20 micrograms/ml). The effects of these endotoxins on the collagen metabolism of the fibroblasts were assessed on the basis of collagen synthesis and collagenase activity. The former was assessed by 3H-proline incorporation and bacterial collagenase digestable protein. The latter was assessed by fibril assay. The results were as follows: There was no change in glucose consumption, cell viability or morphology under the light microscope when the concentration of endotoxin was 20 micrograms/ml or less. 3H-proline incorporation into protein and collagen synthesis were inclined to decrease. Endotoxin from B. gingivalis resulted in an acceleration of collagenase activity. There findings indicate that the endotoxins from these bacteria might affect collagen metabolism early in gingivitis in vivo.
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PMID:[Effects of endotoxins from periodontopathic bacteria on the collagen metabolism of cultured normal human gingival fibroblasts]. 256 64

T-cell subsets extracted from chronically inflamed periodontal tissues were identified using monoclonal antibodies, and their functional activity was analysed using the autologous mixed lymphocyte reaction (AMLR). Tissue was obtained from a total of 33 adult periodontitis (AP) patients and 6 normal/marginal gingivitis (N/MG) patients. All AP patients had received repeated oral hygiene instruction and root planing prior to the surgery, and the majority (30 out of 33) had at least one site with greater than 6 mm loss of attachment from the cementoenamel junction within the surgical field. The N/MG patients had no loss of attachment, and probing depths were less than 3 mm. Single cell suspensions were obtained following collagenase digestion (90 minutes at 37 degrees C) and mechanical disruption of the tissue. T-cell subsets were identified using an indirect immunofluorescence assay on cells obtained from 19 AP patients and the 6 N/MG patients. The mean (+/- standard error) helper:suppressor (T4:T8) ratio for the AP patients was found to be 0.94 +/- 0.48 compared with 1.65 +/- 0.16 for the N/MG group and 1.51 +/- 0.12 for peripheral blood controls. HLA-DR positive macrophages were identified and were found to include both acid phosphatase (AcP) positive and adenosine triphosphatase (ATPase) positive populations. Functional analysis was carried out using cells extracted from the remaining 14 AP patients. Cells from six of these 14 patients were found to be capable of spontaneous proliferation. Co-culture experiments using autologous T and non-T populations revealed that cells from only four patients were able to respond in an AMLR while those from only one of the 14 patients were able to stimulate the AMLR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenotypic and functional analysis of T cells extracted from chronically inflamed human periodontal tissues. 295 90

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 quadrants of the jaw in 2 beagle dogs had various forms of periodontal disease induced by ligatures placed around second, third and fourth premolars in one quadrant and, 2.5 months later, around the same teeth in a second quadrant; gingivitis was allowed to develop in a third quadrant after 4 months; the fourth quadrant served as a healthy control. Crevicular fluid flow, plaque index, gingival index, attachment levels and recession were determined at intervals and collagenolytic activity measured in the fluid. The dogs were killed after 5 months and sections of each site prepared for histomorphometry. Clinically-inflamed and degenerating sites had significantly higher collagenolytic activities (p less than 0.001), lower collagenase inhibitor activities and greater fluid flow than control sites which showed abundant inhibitor activity and minimal active enzyme. Periodontitis sites had higher active enzyme, compared to latent enzyme activities, whereas latent collagenase was predominant in control and gingivitis sites. The collagenolytic activities in periodontitis sites fluctuated with time, suggesting a cyclical pattern. Active enzyme activities correlated strongly with gingival crevicular fluid flow and attachment loss. Periodontitis sites had much more inflammatory-cell infiltration than control and gingivitis sites (p less than 0.001). Thus periodontal disease may be monitored by examination of crevicular fluid collagenolytic enzymes, inhibitors and fluid flow, and these criteria may prove more meaningful than current clinical criteria.
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PMID:Correlation of collagenolytic enzymes and inhibitors in gingival crevicular fluid with clinical and microscopic changes in experimental periodontitis in the dog. 345 36

It is becoming increasingly apparent that the traditional clinical criteria are inadequate for: determining active disease sites in periodontitis, monitoring quantitatively the response to therapy or measuring the degree of susceptibility to future breakdown. In an attempt to develop objective measures, a wide variety of studies have been undertaken using saliva, blood, plaque and gingival crevicular fluid (GCF) as the specimen source. Examination has included: specific bacteria and their products; host cells and their products (enzymatic and antibacterial, both immunologic and non-immunologic); products of tissue injury derived from local epithelial and connective tissues and bone. Although most of the work to date has failed to provide reliable aids to the clinician, refinements in techniques for sampling and the availability of more sophisticated analytic techniques give cause for optimism. Methods proposed for detection of disease-associated bacteria in subgingival plaque vary in their sensitivity and specificity. Dark field microscopy shows some correlation with existing disease; however, the limited specificity of this method imposes severe restrictions on its usefulness. Highly specific polyclonal and monoclonal antisera to suspected pathogens Bacteroides gingivalis and Actinobacillus actinomycetemcomitans have been developed and improved methods of identification of these microbes in plaque by ELISA immunofluorescence and flow cytometry are under development. With respect to the host response, a strong correlation between antibody patterns to specific bacteria and periodontal disease categories appears to be emerging. Although most studies have focused on serum antibody derived from peripheral blood, a shift to detection of local antibody response appears to be likely. Techniques of measurement that are exquisitely sensitive have been developed for detection of major immune recognition proteins such as antibody and complement in crevicular fluid. Research efforts attempting to correlate local antibody response to local disease activity are underway. Measurement of GCF flow rate, endotoxin, H2S, butyrate and a variety of enzymes (e.g., collagenase, arylsulfatase, B-glucuronidase) show good correlation with levels of gingivitis. In periodontitis, the most promising markers of tissue breakdown are prostaglandins of the E series, the enzymes collagenase and aspartate aminotransferase, sulfated glycosaminoglycans, osteoclastic activating factor and bone resorptive capacity of crevicular cells. Assay of the migration of crevicular leucocytes in vivo can serve as an indicator of a defect in host resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indicators of periodontal disease activity: an evaluation. 352 56

Basement membranes in human gingiva are found in dento-epithelial junction, epithelial-connective tissue junction and endothelium-connective-tissue junction where they have important attachment and filtering functions. The ability of plaque and gingiva-derived proteinases to degrade Type IV collagen, the major protein of basement membranes, was examined in vitro. The basement membrane collagen (Type IV) isolated from bovine lens capsules was incubated in the presence of enzyme samples. The degradation was assayed by the release of hydroxyproline from the insoluble substrate and by examining the peptide pattern of the residue by polyacrylamide gel electrophoresis. Salt extracts of inflamed gingival specimens degraded basement membrane collagen into soluble form and produced degradation products that were similar to those produced by human leukocyte extracts. Gingival crevicular fluid collected from patients with severe adult periodontitis also digested the substrate but the degradation pattern was different from the leukocyte and gingival extract samples. The pattern closely resembled the degradation produced by bacterial plaque extracts. A third type of cleavage was observed when collagenase from Clostridium histolyticum was incubated with basement membrane collagen. Crevicular fluid and the extracts from gingiva, leukocytes and plaque also contained gelatinase and elastase-like enzyme activities that have earlier been shown to be potent in degrading basement membrane. It was concluded that enzymes capable of degrading basement membrane collagen in gingivitis and periodontal disease may originate from both plaque bacteria and human leukocytes. It also appeared that the enzymes responsible are more likely to be gelatinase and elastase-like enzymes than specific collagenases.
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PMID:Degradation of basement membrane collagen by proteinases from human gingiva, leukocytes and bacterial plaque. 631 10

Interleukin-1 beta (IL-1 beta) may be related to the pathological processes associated with periodontitis, primarily due to its ability to induce collagenase, increase neutrophil chemotaxis, and stimulate bone resorption. This study was designed to histologically quantitate IL-1 beta positive cells from various histologic fields in untreated gingivitis/early periodontitis (G/EP) versus moderate/severe periodontitis (M/SP) gingival tissues, and associate these with collagen loss. Two gingival biopsies from 8 patients were collected, one from a G/EP site and one from a M/SP site. Mouse monoclonal antibodies in combination with an avidin-biotin-peroxidase system were used to stain for IL-1 beta, while the van Gieson method was used to stain for collagen in serial sections. Collagen loss in G/EP (35%) and M/SP (52%) fields was consistent with gingivitis and periodontitis, respectively. IL-1 beta positive cells in combined coronal/sulcular (Co/Su) and apical/sulcular (Ap/Su) fields (nearest the bacterial insult) were significantly more numerous compared to combined coronal/middle (Co/Mi) and apical/middle (Ap/Mi) fields (p < 0.05). While numbers and percentages of IL-1 beta positive cells were generally higher in M/SP biopsies, differences were not significant. Further, there was no correlation between the number of IL-1 beta positive cells and percent collagen loss. However, a significant correlation between IL-1 beta positive cells and corresponding gingival crevicular fluid IL-1 beta concentrations was noted (r = 0.65, p = 0.01). Through the use of immunohistochemistry, this study demonstrated that the presence of IL-1 beta + cells does not appear to have a direct association with collagen loss.
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PMID:Histological evaluation of interleukin-1 beta and collagen in gingival tissue from untreated adult periodontitis. 750 86

The ability of stromelysin (SL), fibroblast-type collagenase (FIB-CL) and tissue inhibitor of metalloproteinases (TIMP), to differentiate between healthy, gingivitis and periodontitis sites was investigated. SL and FIB-CL are members of a family of enzymes which are capable of degrading most of the extracellular matrix macromolecules. Extracellular control of these enzymes is performed by TIMP. 40 patients each provided 3 GCF samples from healthy, gingivitis and periodontitis sites. GCF samples were collected by means of sterile paper strips. GCF samples were eluted into 500 microliters of assay buffer and assays for SL, FIB-CL and TIMP were performed by a sandwich ELISA. The mean amounts of SL and TIMP in diseased sites (gingivitis and periodontitis) were significantly higher than the mean amount of these GCF components in healthy sites (MANOVA p values were: 0.006 for SL and 0.001 for TIMP). GCF SL and TIMP differentiated healthy from diseased sites. Both SL and TIMP showed moderate correlation with clinical indices. FIB-CL was detectable in only 20.8% of all sites and did not correlate with disease status.
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PMID:Gingival crevicular stromelysin, collagenase and tissue inhibitor of metalloproteinases levels in healthy and diseased sites. 756 Feb 32

The purpose of this study was to compare, using cell blot analysis, the association of gingival tissue mononuclear cells (GTMC) isolated from lesions displaying histories of early-onset periodontitis (EOP; typically B-lymphocyte dominated) and gingivitis (typically T-lymphocyte dominated) with the B-cell stimulating cytokine, interleukin (IL)-4, and the T-cell stimulating cytokine, IL-2. Eleven EOP patients and 11 age- and gender-similar gingivitis control (GC) subjects participated. Gingival tissue adjacent to the alveolar crest normally removed during surgery was digested in collagenase-containing media and GTMC were isolated by density gradient centrifugation. Cells were separated into four aliquots. One was left unstimulated; the remainder were stimulated for 2 hours with Porphyromonas gingivalis outer membrane protein, mitogen Concanavalin A, or common antigen tetanus toxoid. Cells then were centrifuged onto transfer membranes and incubated in RPMI 1640 media for 6 hours to allow absorption of secreted cytokine. Membranes were treated with monoclonal anti-IL-2 or anti-IL-4, followed by a biotin-conjugated second layer, streptavidin-alkaline phosphatase and nitro blue tetrazolium/5-bromo-4-chloro-indolyl-phosphate (NBT/BCIP) color development. A higher percentage of GTMC from EOP patients were IL-2+ when stimulated with P. gingivalis compared with GTMC from GC patients (20 +/- 2% vs. 12 +/- 2%, P < 0.003). A higher percentage of non-stimulated GTMC from EOP patients produced IL-4 than from GC (22 +/- 4% vs. 6 +/- 3%, P < 0.00007), as well as when stimulated with P. gingivalis (22 +/- 3% vs. 13 +/- 2%, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gingival cell IL-2 and IL-4 in early-onset periodontitis. 799 15


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