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)

Cells expressing messenger RNA (mRNA) for inflammatory cytokines [interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha), IL-6, IL-8] were demonstrated by in situ hybridization in human inflamed gingiva. When this technique was used in conjunction with immunohistochemistry, IL-1 alpha and/or beta and IL-8 messages were observed predominantly on macrophages infiltrating the gingiva. TNF-alpha messages were abundant on macrophages and T cells. In contrast, the IL-6 mRNA were more widely distributed on many types of cells such as macrophages, T cells, fibroblasts, endothelial cells and B cells. This study clearly identified the cells which express mRNA for inflammatory cytokines in inflamed gingiva and suggested an involvement of cytokine network in the generation of human periodontitis.
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PMID:Detection of inflammatory cytokine messenger RNA (mRNA)-expressing cells in human inflamed gingiva by combined in situ hybridization and immunohistochemistry. 162 99

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

Interleukin-1 (IL-1)-producing cells in inflamed gingival tissues obtained from patients with periodontitis were examined by combined immunohistochemistry and in situ hybridization. Macrophages, T cells, B cells, and endothelial cells were visualized in the lesions by the immunoperoxidase method using specific antibodies to each cell type. Subsequent in situ hybridization using 35S-labeled synthetic oligonucleotide probes complementary to human IL-1 alpha and IL-1 beta mRNA showed IL-1 transcripts in macrophages predominantly but not in T cells or B cells. Neither fibroblasts nor keratinocytes contained the IL-1 message to any significant extent. Endothelial cells also were essentially negative for IL-1 messages. These findings indicate that IL-1 is produced principally by macrophages in inflamed gingival tissues of humans.
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PMID:Interleukin-1 mRNA-expressing macrophages in human chronically inflamed gingival tissues. 205 89

Samples of gingival crevicular fluid (GCF) were harvested from sites manifesting features characteristic of active disease including inflammation, periodontal attachment loss, and radiographic signs of alveolar bone destruction in untreated patients with advanced periodontitis. The presence and concentrations of interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) were measured using ELISAs specific for these cytokine molecules. IL-1 alpha and/or IL-1 beta were identified in the GCF of 15 of 15 patients having untreated periodontitis. Ninety percent (71 of 79) of the sites tested contained measureable amounts of IL-1, with IL-1 beta as the more frequently occurring form. IL-1 alpha levels ranged from 0.23 nM to 13.9 nM in the GCFs. IL-1 beta levels were between 0.04 nM and 5.28 nM. Marked reductions of total IL-1 levels were observed following effective treatment. Both forms of IL-1 messenger RNA (mRNA) were detected in 17 of 17 gingival tissue samples from 6 patients. These results demonstrate that IL-1 is produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 may serve as a marker of periodontal tissue destruction.
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PMID:Measurement of interleukin-1 alpha and -1 beta in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 214 75

A significant level of interleukin-1-(IL-1)-like activity was detected in gingival crevicular fluid obtained from sites in patients with chronic inflammatory periodontal disease, confirming a previous report of IL-1-like activity detected in human gingival crevicular fluid from patients with chronic inflammatory periodontitis (J. A. Charon, T. A. Luger, S. E. Mergenhagen, and J. J. Oppenheim, Infect. Immun. 38:1190-1195, 1982). In the present study, we sought to investigate whether this IL-1-like activity belonged to IL-1 alpha or IL-1 beta and to characterize some of the biochemical properties of this factor. Polyclonal antibodies against recombinant human IL-1 alpha or IL-1 beta (rIL-1 alpha or rIL-1 beta) have been used for serological comparison of the IL-1-like factor. IL-1-like activity was completely neutralized by anti-human rIL-1 alpha antiserum, but not by anti-human rIL-1 beta antiserum. On gel filtration with a high-pressure liquid chromatographic Superose 12 column, IL-1-like activity was separated into two peaks, one with a molecular weight of about 43,000 and the other with a molecular weight of less than 17,000. The majority of the IL-1-like factor with a low molecular weight in human gingival crevicular fluid migrated at a molecular weight of about 17,000 under the reducing conditions of sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The specificity of the IL-1-like factor was further confirmed by an immunochemical method (Western blotting [immunoblotting]) by using anti-human rIL-1 alpha monoclonal antibodies. On isoelectric chromatography with a high-pressure liquid chromatographic Mono P column, the pI of this IL-1-like factor was between pH 4.9 and 5.2. These results suggest that the IL-1-like factor in human gingival crevicular fluid from diseased sites in patients with chronic inflammatory periodontitis consists predominantly of IL-1 alpha.
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PMID:Partial characterization of an interleukin-1-like factor in human gingival crevicular fluid from patients with chronic inflammatory periodontal disease. 219 29

It seems to be generally agreed that periodontal disease is a local manifestation of a systemic immune response. Interleukin-1 (IL-1), which has multiple biologic activities, is detected in the gingival sulcus fluid of periodontitis sites. Recent investigations have revealed that IL-1 and tumor necrosis factor (TNF) are analogous to osteoclast activating factor and promote bone resorption. These findings have suggested the possibility that IL-1 and TNF may play a significant role in the initiation and development of periodontal disease. However, it remains to be determined whether these cytokines influence periodontal tissue breakdown in periodontitis. To elucidate the mechanisms of tissue breakdown in periodontitis, we examined cytokine production by human periodontitis gingival tissue. Twelve periodontitis patients were included in this study. Control subjects with healthy periodontium consisted of nine individuals. Gingival samples were biopsied from inflamed or healthy gingival tissues. Biopsy specimens were dissected into fragments 3 mm in diameter and plated onto 24 well culture plates with RPMI 1640 medium. IL-1 activity was measured by a growth inhibition assay using melanoma cell line A 375. An enzyme-linked immunosorbent assay (ELIZA) was used for measuring levels of human IL-1 alpha, IL-1 beta. TNF alpha activity was measured by a growth inhibition assay using cell line LM2D6. IL-1 activity was detected in significantly (p less than 0.001) higher levels in culture supernatants from gingival tissues in periodontitis (48.0 +/- 23.3 units/ml) than in control tissues (2.3 +/- 0.6 units/ml), however, levels of IL-1 activity were not associated with periodontal pocket depth or extent of alveolar bone resorption in periodontitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of cytokine production in inflamed human gingival tissues in periodontitis. Interleukin-1 (IL-1 alpha, beta) and tumor necrosis factor (TNF alpha)]. 248 32

The role of the polymorphonuclear leukocyte (PMNL) as a primary protective cell in periodontal diseases has been well recognized. Functional abnormalities of PMNL chemotaxis have been implicated in the pathogenesis of some types of periodontitis. However, no consistent correlation with other PMNL functions has been reported. In the present study, phagocytosis and intracellular killing (oxidative product formation) of the PMNL from the patients with various forms of periodontal disease were evaluated by flow cytometry. Moreover, interleukin 1 (IL-1) production by the PMNL was determined by means of the enzyme-linked immunosorbent assay (ELISA) with monoclonal antibodies against rIL-1 alpha and rIL-1 beta. In order to examine these functions of peripheral (p-PMNL) and/or gingival crevicular PMNL (g-PMNL), 15 patients with localized juvenile periodontitis (LJP), 13 patients with generalized juvenile periodontitis (GJP) and 52 patients with adult periodontitis (AP) served as subjects. About 50% of the patients in LJP and GJP group exhibited depressed p-PMNL phagocytosis. While only a minimal number of the AP patients and no healthy subjects showed any reduction of p-PMNL phagocytosis. The reduction of phagocytosis was not related to the clinical periodontal status, and no detectable improvement of p-PMNL phagocytosis could be observed after periodontal therapy. In addition, it was suggested that complement receptors on the p-PMNL might be closely related with the reduction. Compared to p-PMNL, g-PMNL from the same individual have a lower phagocytic capacity in all subjects. However, no significant difference in g-PMNL phagocytosis could be demonstrated among three patient groups. Incremental oxidative responses in p-PMNL were observed in LJP, GJP and AP patients without any significant difference being found among these three groups. The increased rate of oxidative product formation was related to the clinical periodontal status, and it followed that periodontal therapy had significant effect on the improvement of this p-PMNL function. In IL-1 production assay of PMNL, a significant amount of IL-1, especially IL-1 beta, was observed in g-PMNL, but not in p-PMNL. The g-PMNL of the patients was found to produce greater amounts of IL-1 alpha and IL-1 beta than did the healthy controls. In addition, IL-1 production of p-PMNL was induced by the stimulation with some pathogenic bacteria including Bacteroides gingivalis. These results suggest that impaired PMNL phagocytosis may contribute to the early onset of periodontal deterioration in some young patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Phagocytosis, intracellular killing and interleukin 1 production of polymorphonuclear leukocytes in human periodontal diseases]. 263 96

Endothelial cell activation by endotoxin (LPS), tumor necrosis factor (TNF), Interleukin-1-alpha, beta (IL-1-alpha, beta) and phorbolesters (TPA) results in increased monocyte adhesion. Examination of kinetics of monocyte adhesion shows that the onset of adherence enhancement (AE) is similar in all five agents (about 300% AE at 6 h), while its decrease is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced activation (LPS versus IL-1-beta:260% versus 60% at 18 h). Monoclonal antibody (4D10), raised against 24 h LPS-stimulated endothelial cells detects an endothelial cell-specific activation antigen at Mr 81,000 that is induced by LPS, TNF, IL-1-alpha, beta and TPA (within 6 h about 100% positive cells). Decrease in antigen-positive cells is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced antigen expression (LPS vs. IL-1-beta: 60% vs. 5% at 24 h). In situ the antigen is not expressed in normal and chronic inflammatory tissues. Acute inflammatory tissues, including contact and atopic dermatitis, psoriasis and periodontitis, however, show endothelial cells staining strongly positive. In contact eczemas at different times after elicitation (0, 6, 24, 72, 96 h), expression of the antigen is first seen after 24 h and is still strong at 96 h. These data indicate that LPS/TNF conduct an endothelial cell activation program in vitro, showing the same prolonged kinetics that is found for endothelial cell activation in the acute inflammatory process in vivo.
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PMID:Characterization and expression kinetics of an endothelial cell activation antigen present in vivo only in acute inflammatory tissues. 331 46

Periodontitis is a general term for disease categories, including juvenile periodontitis (JP), rapidly progressive periodontitis (RPP), and adult periodontitis (AP), which may or may not share a common etiology and pathogenesis. These disease categories are characterized by differences in progression of tissue destruction and differences in age group susceptibility, but not, to our knowledge, by differences in cytokine responses of inflammatory cells. The present study examined blood cell counts and interindividual variation in the ability of PBMC of patients in three different categories of periodontitis to produce cytokines after stimulation with different oral bacterial species in vitro. The AP group had a significantly lower production of IL-1ra when stimulated with Porphyromonas gingivalis (P.g.) and Actinobacillus actinomycetemcomitans (A.a.) (P < 0.05). Streptococcus sanguis (S.s.), which is associated with normal periodontal conditions, induced extremely high levels of IL-1 alpha and TNF alpha production in all groups. The RPP group had a significantly higher number of monocytes (MC) than the AP group (P < 0.05). Additionally, JP patients had a significantly higher concentration of polymorphonuclear granulocytes compared to juvenile controls (P < 0.05). In conclusion, IL-1 alpha, TNF alpha, or IL-6 production by peripheral blood MC after in vitro stimulation with oral bacterial type stains may not distinguish different categories of periodontitis. The results support the hypothesis that the cytokine IL-1ra is produced in different concentrations in the two groups: RPP and AP. Furthermore, elevated MC concentration in the RPP group compared to the AP group may be an important pathogenic feature in RPP.
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PMID:Bacterial-stimulated cytokine production of peripheral mononuclear cells from patients of various periodontitis categories. 773 Sep 65

The capacity of mononuclear blood cells to produce interleukin-1 alpha (IL-1 alpha) after stimulation with Porphyromonas gingivalis in cell culture was studied. The results obtained with cells from periodontitis patients were compared with those from a control population. The concentration of IL-1 alpha in serum and saliva was also determined and compared with the concentration in mononuclear blood cell cultures. No significant relationship was found between the incidence of periodontitis or severity of the lesions and IL-1 alpha production in the presence of P. gingivalis. Nevertheless, 11 of 30 periodontitis patients, showed levels > 30 pg/ml of IL-1 alpha in mononuclear blood cell cultures stimulated by P. gingivalis, whereas only three healthy control showed these titers of IL-1 alpha.
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PMID:Induction of interleukin-1 alpha production by Porphyromonas gingivalis in mononuclear blood cell cultures from periodontitis patients. 788 Dec 68


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