Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter rectus is one of the predominant bacteria in the lesions of human periodontitis. The surface antigens of the bacterium contain several components which may play significant roles in colonization and pathogenesis. A high-molecular-weight protein was selectively isolated from the cell surface of C. rectus by acid extraction and purified by DEAE Sepharose. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis showed that the extracted protein was 150 kDa. The protein was not found in Campylobacter curvus ATCC 35224 or Wolinella succinogenes ATCC 29543. Lipopolysaccharide (LPS) was extracted from various C. rectus strains by the hot phenol-water method. SDS-PAGE patterns revealed that C. rectus LPS was the smooth type in nature. Monoclonal antibodies against C. rectus were generated by the fusion of SP2/0 myeloma cells with splenocytes from BALB/c mice immunized with whole cells of C. rectus ATCC 33238 strain. An Immunoglobulin G1 monoclonal antibody reacted with the high-molecular-weight proteins from 4 of 9 C. rectus strains, indicating that the 150 kDa protein exhibits antigenic heterogeneity. Immunoelectron microscopic study revealed that the monoclonal antibody recognized the S-layer of C. rectus cells. An IgM monoclonal antibody reacted with LPSs from C. rectus strains at molecular weights between approximately 20.0 kDa and 24.0 kDa. The monoclonal antibody did not react with any other LPSs from C. curvus ATCC 35224 or W. succinogenes ATCC 29543. The reactivities of this monoclonal antibody indicate that it recognizes an O-specific side chain epitope of C. rectus LPS. Sera from patients with adult periodontitis showed strong reactivity with the 150 kDa protein antigen and LPS from C. rectus strains. As determined by immunoblotting analysis, sera from periodontally healthy individuals, however, showed little or no reactivity. The levels of serum IgG antibodies of patients with periodontitis to the protein antigen and LPS were statistically significantly higher than those of periodontally healthy individuals, as assessed by an enzyme-linked immunosorbent assay.
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PMID:Analysis of cell surface antigens of Campylobacter rectus. 130 24

Polymorphonuclear leukocytes (PMNs) have been implicated in the pathogenesis of inflammatory gingivitis and periodontitis. To further study the role of PMNs in mediating gingival injury, we cocultured these cells in vitro with monolayers of human gingival epithelial cells. Scanning electron microscopy revealed that the epithelial cells were homogeneous and SDS-PAGE/immunoblot analysis identified the presence of keratins K3, K13 and the K6/16 pair which authenticated the oral origin of the cells. Injury to the gingival cells was determined by scanning electron microscopy and measurement of cell detachment and cytolysis. Unstimulated PMNs produced minimal lysis or detachment, but PMNs stimulated by phorbol myristate acetate produced marked epithelial cell detachment without lysis, which was time- and PMN-dose-dependent. Supernatants of activated PMNs were similarly effective, indicating that the mediator was a stable soluble substance. Elastase and cathepsin G, two neutral proteases of PMN origin, produced time- and concentration-dependent detachment of gingival epithelial cells, suggesting that these enzymes may mediate this form of injury. In other studies, gingival epithelial cells were exposed to PMN myeloperoxidase (MPO), chloride and glucose plus glucose oxidase (GO) as a hydrogen peroxide (H2O2) generating system. The toxic oxygen species produced by this system caused lysis of the epithelial targets which was dependent on the duration of incubation and the concentrations of MPO and GO. Azide, an inhibitor of MPO, and catalase, a scavenger of H2O2, inhibited the lytic activity of this system. Scanning electron micrographs of gingival epithelial cells cocultured with activated PMNs showed lifting of the cells from the plating surface, while target cells attacked by the MPO system revealed extensive damage of cell membranes. These studies indicate that activated PMNs cause nonlytic detachment injury to gingival epithelial cells which may be mediated by digestion of their extracellular matrix by granule neutral proteases. Furthermore, PMN MPO is capable of generating toxic oxygen species which can lyse these epithelial cells. Collectively, these actions could have profound adverse effects on the function and integrity of the gingival epithelium.
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PMID:Neutrophil-mediated damage to human gingival epithelial cells. 131 Oct 41

Previous reports have suggested that active progression of periodontitis may be correlated with increased collagenolytic activity, and that improved clinical conditions after tetracycline treatment may be explained by inhibition of host collagenase. Eighty-two patients with a recent history of periodontal abscesses and/or loss of gingival attachment level (GAL) despite active periodontal therapy were enrolled in a double-blind, randomized, placebo-controlled trial. Clinical measurements, sampling of gingival crevicular fluid (GCF) and subgingival scaling were performed every 2 months. If any site exhibited greater than 2 mm loss of GAL or a periodontal abscess, patients were administered either 100 mg doxycycline per day for 3 weeks or placebo. During 12 months of monitoring, 55 patients exhibited recurrent active disease and were then randomly assigned to either the doxycycline (n = 30) or placebo (n = 25) groups. Analysis of active collagenase and latent collagenase in GCF samples were determined by functional assays and quantitated after SDS-PAGE and fluorography. Collagenase activities were assayed at sites exhibiting active destruction (study site), at sites with pocket depth comparable to the study site but without active destruction, and at healthy sites. Clinical measurements of GAL and collagenase activity were made at intervals between 1 wk and 7 months after completion of the drug regime. Within 7 months, 15 out of 19 patients on placebo exhibited recurrent disease compared to 13 out of 29 patients on doxycycline. Collagenase activity exhibited large variations among patients and was analyzed as presence or absence of active collagenase with a logistic model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Collagenase activity in recurrent periodontitis: relationship to disease progression and doxycycline therapy. 166 66

The antigens from outer membrane protein extracts of Porphyromonas gingivalis (W50), grown under different haemin concentrations, were examined for binding with serum antibodies from patients with severe progressive periodontitis or from periodontally healthy control subjects. P. gingivalis was grown under haemin limitation (0.33 micrograms/ml) and haemin excess (2.5 micrograms/ml) conditions in a chemostat at a mean generation time of 6.9 h, at pH 7.5. Sarkosyl-insoluble fractions of outer membrane proteins from P. gingivalis were prepared, and analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblot techniques. The SDS-PAGE analysis of the outer membrane of haemin-limited P. gingivalis identified several new protein components, or changed expression of bands compared with cells grown under haemin excess. Immunoblot analysis showed IgG antibodies to 2 haemin deprivation-induced proteins in patients with severe progressive periodontitis, but not in the control sera. These results confirm the immunogenicity of some of the haemin-regulated outer membrane proteins of P. gingivalis in severe progressive periodontitis.
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PMID:The immunogenicity of outer membrane proteins of haemin-depleted Porphyromonas (Bacteroides) gingivalis W50 in periodontal disease. 166 47

Crevicular fluid (CF) analysis is a potential tool for site-specific diagnosis of periodontal disease activity. In this study, CF was collected using a novel washing method from 91 sites in 18 adult periodontitis patients both before and after conventional periodontal treatment. The sites studied were classified according to their clinical status and the number of polymorphonuclear leukocytes (PMN's) in CF samples. CF proteins were analyzed from individual sites with gel electrophoresis (SDS-PAGE). Furthermore, both the cell-bound and soluble neutral proteolytic activities of the samples were determined. Albumin was the main protein both in healthy and slightly inflamed sites. The most severely inflamed sites were characterized by high levels of low molecular weight (LMW) proteins (mol. weight ca. 12,000) and strong cell-bound neutral proteolytic activity. Scaling and root planing reduced both the LMW proteins and neutral proteolytic activity markedly in pockets responding well to treatment. The levels of the LMW proteins in CF correlated with the cell-bound neutral proteolytic activity, which reflected the number of PMN's in the sample. The present results suggest that the appearance of the LMW proteins in CF is associated with the periodontal inflammatory status of the site.
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PMID:Protein composition of crevicular fluid before and after treatment. 175 42

Soluble antigenic preparations of Veillonella parvula and Bacteroides gingivalis were separated by SDS-PAGE and used after electroblotting and solubilization for in vitro lymphocyte stimulation in 13 patients with severe periodontitis and 12 controls. The cellular responses of controls and patients to V. parvula antigens were represented by four main proliferation-inducing fractions with 74-66, 52-46, 22-19 and 12 kD mol. wt. These fractions induced slightly enhanced DNA synthesis in lymphocytes from eight patients who failed to respond to whole antigenic extract. Lymphocyte samples from Veillonella whole extract unresponsive patients were also examined for in vitro proliferation by B. gingivalis fractions. Almost all stimulatory activities could be classified into five regions of 84-74, 35-31, 28-25, 17-15 and 12 kD.
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PMID:T cell proliferative responses to molecular fractions of periodontopathic bacteria. 198 18

Outer membrane proteins (OMPs) were extracted from whole cells of several Porphyromonas and Prevotella strains and their OMPs profiles were examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The SDS-PAGE analysis revealed that OMP profiles of Porphyromonas and Prevotella strains show species-specific patterns and P. gingivalis characteristically had two kinds of major outer membrane proteins (MOMPs). A 53 Kd MOMP from P. gingivalis FDC 381 and a 67 Kd MOMP from ATCC 33277 were purified. Sera from periodontitis patients and healthy subjects were analyzed for immunoreactivities against both the purified MOMPs of P. gingivalis by immunoblotting analysis. The sera from 18 patients reacted to the 53 Kd MOMP, 10 to the 67 Kd MOMP, and only three sera reacted to both MOMPs. The sera of healthy subjects also reacted, but weakly, to either the 53 Kd or 67 Kd MOMP. The SDS-PAGE OMP profiles prepared from 13 clinical isolates of P. gingivalis and immunoblotting analysis of human sera against the two kinds of P. gingivalis MOMPs indicate that periodontal diseases resulting from P. gingivalis are initiated and sustained by at least two MOMPs of P. gingivalis.
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PMID:Purification and characterization of two major outer membrane proteins from Porphyromonas gingivalis. 209 88

Gingival crevicular fluid (GCF) is a promising source for markers of destructive periodontal diseases activity. As the initial stage of a longitudinal study into the characterization of disease markers, GCF sampled from 104 sites in 74 adolescents was examined via sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS/PAGE). In this population, which had varying degrees of gingivitis but little evidence of destructive periodontitis, there was a highly homologous GCF protein profile. The plasma components, albumin, transferrin and IgG, were major constituents of all samples. In addition, a second group of non-plasma derived proteins, with molecular weights 37 kDa, 47 kDa, 57 kDa and 59 kDa, was also commonly detected. The high frequency of occurrence of these components suggests that they may represent products of normal turnover of the periodontal tissues. Analysis of GCF sampled from patients with progressing destructive disease revealed a different SDS/PAGE profile particularly with respect to proteins of non-plasma origin. It is anticipated that the major metabolic changes which accompany the destruction of the tissues during future disease episodes in the adolescent study population will be discernible as alterations to the GCF protein profile.
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PMID:The protein composition of gingival crevicular fluid sampled from male adolescents with no destructive periodontitis: baseline data of a longitudinal study. 213 72

Saliva collected from subjects with healthy and with diseased periodontium was assayed for collagenase activity by incubation at 25 degrees C with soluble type I, II or III collagen. The degradation products were analyzed by separation in SDS-polyacrylamide gel electrophoresis followed either by protein staining or by exposure of the dried gel to X-ray film in the case of radioactively labeled type I collagen. Collagenase of vertebrate type was detected in the whole saliva of all subjects but not in parotid, sublingual or submandibular fluids. Most of the collagenase was in the soluble fraction of saliva that also contained factors which both activated and inhibited the enzyme. The salivary collagenase resembled the collagenase of human PMNs and gingival sulcular fluid in its molecular size of 70,000 daltons, in its activation by gold thioglucose and in its tendency to degrade types I and II collagens over type III collagen. Before periodontal treatment, the saliva of periodontitis patients had significantly higher collagenase than after treatment. In periodontitis, collagenase existed mainly in the active form, while in the healthy mouths most of the enzyme was latent but could be activated by sulfhydryl reagents or proteolytically with trypsin, and chymotrypsin but not by human plasma kallikrein or plasmin. In some of the samples from untreated periodontitis patients bacterial collagenase may have been present in small quantities. Most of the collagenase in the saliva from all subjects appeared to originate from PMNs entering the oral cavity through the gingival sulcus.
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PMID:Salivary collagenase. Origin, characteristics and relationship to periodontal health. 216 44

In previous studies, elevations in the levels of active and latent collagenase in gingival crevicular fluid (GCF) have been correlated positively with periodontal disease activity. To provide a simple diagnostic approach for testing collagenolytic activity, the feasibility of using a 3.0 ml water mouthrinse to collect GCF simultaneously from all sites in the mouth was assessed. Patients with adult periodontitis (AP, n = 23) and local juvenile periodontitis (LJP, n = 7) were sampled before periodontal therapy and some (12 AP, 4 LJP) were also assessed longitudinally after scaling and root planing, administration of antibiotics, and following periodontal surgery. Healthy patients (n = 19) were used as controls. The levels of active collagenase, procollagenase, and collagenase inhibitor activity were determined by functional assays and quantitated after SDS-PAGE and fluorography. Gelatinase and progelatinase were assayed by enzymography on gelatin-substrate gels. Active collagenase levels were found to be significantly higher (14- to 20-fold) in AP and LJP patients compared to controls, whereas matrix metalloproteinase activity was not detected in mouthrinses from edentulous patients. Collagenase inhibitor levels were generally low in all groups of subjects tested. Following clinical treatment the levels of active collagenase and gelatinase were reduced; the reduction was significant for active collagenase after tetracycline treatment and scaling in LJP patients. Of the clinical indices recorded (gingival index, plaque index, and pocket depth) there were no significant correlations with enzyme activity but similar trends were observed between the changes in active collagenase and gingival index. In patients with untreated periodontal disease, collagenase occurred predominantly in the active form. N-ethylmaleimide (NEM) and p-aminophenylmercuric acetate (AMPA) were equally effective as activators of the latent collagenase, indicating that the collagenase was derived from PMNs, which were also the source of gelatinase. The results of these studies indicate that measurement of active collagenase and gelatinase in mouthrinse samples is potentially useful in the diagnosis and assessment of periodontal disease activity.
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PMID:Identification of polymorphonuclear leukocyte collagenase and gelatinase activities in mouthrinse samples: correlation with periodontal disease activity in adult and juvenile periodontitis. 217 Jun 17


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