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)

Interleukin-1(IL-1), a cytokine present in the gingiva and crevicular fluid of patients with periodontitis and in the periodontal ligament (PDL) of experimentally moved teeth, has multiple biological activities, including the ability to elicit bone resorption. Interleukin-6, also found in the gingiva of patients with periodontitis, may induce osteoclastic bone resorption through an effect on osteoclastogenesis. Here IL-6 production and its gene expression in response to recombinant IL-1 beta were examined in primary cultures of PDL cells. IL-1 beta stimulated IL-6 production by these cells in a dose- and time-dependent manner; this increase in IL-6 production was much higher than that in human gingival fibroblasts. In situ hybridization, using a synthetic oligonucleotide DNA probe of the IL-6 gene, revealed that most PDL cells expressed IL-6 mRNA in response to IL-1 beta treatment. The finding that IL-6 is produced by PDL cells and is regulated by IL-1 beta has revealed a potentially important mechanism for controlling alveolar bone resorption.
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PMID:Stimulation by interleukin-1 of interleukin-6 production by human periodontal ligament cells. 141 23

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

We have estimated the levels of Interleukin-1 beta (IL-1 beta) by ELISA in gingival crevicular fluid (GCF) at 58 sites from 37 patients with adult periodontitis. GCF was collected for 5 s on filter papers and a 2nd sample was collected for 30 s 1 min later. 68/116 strips yielded detectable levels of IL-1 beta. IL-1 beta was present in both the 1st and 2nd samples at 28 sites, in the 1st only at 4 sites and in the 2nd only at 8 sites; 18 sites were below the level of detection for the assay. When the concentrations of IL-1 beta were calculated in the original volume of GCF on each strip, the mean value for positive strips was 34.16 +/- 29.45 (SD) pg/microliters with a range from 1.75 to 97.13 pg/microliters. There were no statistically significant correlations with the plaque index, bleeding index or probable crevice depth (pocket depth). The results indicate that IL-1 is present in the GCF from a proportion of sites with evidence of previous periodontal destruction.
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PMID:Interleukin-1 beta (IL-1 beta) levels in gingival crevicular fluid from adults with previous evidence of destructive periodontitis. A cross sectional study. 173 10

Interleukin 1 beta is a potent bone resorptive cytokine which also mediates soft tissue destruction through the stimulation of prostaglandin production, and the induction of collagenase and other proteases. This constellation of activities suggests a role for IL-1 beta in the pathogenesis of human periodontitis. Levels of IL-1 beta were therefore determined in tissue obtained from (1) diseased, active (2) diseased, inactive and (3) healthy sites from 12 patients with destructive adult periodontitis. Disease activity was defined as attachment loss of greater than or equal to 2.5 mm, as determined by sequential probing and the tolerance method. IL-1 beta was extracted from homogenates of tissue biopsies taken at surgery, and levels were quantified by ELISA. IL-1 beta was found to be present in most patient tissue samples, with levels ranging from 0-82 ng/ml. Disease active sites had higher IL-1 beta levels (p less than 0.05) than inactive and healthy sites. Diseased inactive sites were divided into 2 groups, those losing small amounts of attachment (0.5-2.0 mm, worsening sites) and those which showed no change or attachment gain (stable sites). Stable diseased sites had IL-1 beta levels which were comparable to those found in healthy sites, and which were significantly different from active sites (p less than 0.02). Worsening sites had IL-1 beta levels intermediate between the levels in stable and active sites. Detection of disease activity occurred more frequently at sites with IL-1 beta levels greater than 25 ng/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Levels of interleukin 1 beta in tissue from sites of active periodontal disease. 189 50

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

The extracellular release of IL-1 beta by cultured peripheral blood monocytes from 26 periodontitis patients and 26 control subjects was measured by radioimmunoassay. Unstimulated monocytes from periodontitis patients released significantly more IL-1 beta than controls during 24 h of culture; there was a wide variation in the amount of IL-1 beta released (0.45-13.00 ng/ml per 10(6) cells) which did not correlate with either the degree of bone loss or pocket formation observed clinically. When stimulated with lipopolysaccharide (LPS; Actinobacillus actinomycetemcomitans; 5 micrograms/ml) monocytes from periodontitis patients produced significantly more IL-1 beta than those from control subjects. Monocyte culture supernatants from another 10 periodontitis patients and 10 control subjects were also assayed for both IL-1 beta and TNF-alpha by enzyme-linked immunosorbent assays. Spontaneous and LPS-stimulated (Bacteroides gingivalis; 5 micrograms/ml) IL-1 beta release were again significantly higher for periodontitis patients. TNF-alpha was detected in the periodontitis cultures (0-765 pg/ml per 10(6) cells), but the mean value was not significantly different from controls. LPS-stimulated TNF-alpha release, however, was significantly higher than for control subjects, and there was a strong correlation between spontaneous IL-1 beta and TNF-alpha release by monocytes from the periodontitis group. Measurement of interferon-gamma (IFN-gamma) in lymphocyte cultures from these patients by immunoradiometric assay showed that IFN-gamma levels in periodontitis cultures were consistently low, but not significantly so when compared to controls; both groups responded equally to concanavalin-A (5 micrograms/ml). Although the precise roles of IL-1 beta and TNF-alpha in periodontitis remain unclear, these data provide evidence that both cytokines may participate in the pathogenesis of the disease.
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PMID:The release of interleukin-1 beta, tumor necrosis factor-alpha and interferon-gamma by cultured peripheral blood mononuclear cells from patients with periodontitis. 214 29

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

Lipopolysaccharide responsiveness in human subjects was assessed through the examination of LPS-stimulated PGE2 and IL-1 beta release from counterflow isolated monocytes from patients with varying levels of periodontal destruction. This study was performed in order to investigate a possible relationship between LPS-mediated secretory responses in monocytes and susceptibility to periodontal destruction in humans. Subjects were chosen based on apparent resistance or susceptibility to disease as measured by little or no periodontal destruction versus generalized severe destruction, respectively. Because IFN-gamma can influence LPS-stimulated responses, the effect of IFN-gamma on the LPS-stimulated release of PGE2 and IL-1 beta was also assessed. Peripheral blood monocytes were separated by counterflow centrifugation and cultured (10(6)/ml/well) with control medium or medium containing LPS from Bacteroides gingivalis, B. intermedius, Actinobacillus actinomycetemcomitans, or Salmonella typhimurium, with or without 10 Units/ml recombinant IFN-gamma. Media were exchanged at 24 and 48 hours and culture supernatants assayed for both PGE2 and IL-1 beta by RIA. Patients classified as Susceptible to periodontitis demonstrated 2- to 3-fold greater PGE2 release than Resistant patients. This difference was observed with all LPS preparations over both the 0-24 hour and 24-48 h culture periods. IL-1 beta release, however, was not significantly different between patient groups. IFN-gamma did not affect the LPS-stimulated release of PGE2 but significantly enhanced the release of IL-1 beta. The IFN-gamma effects were similar for both patient groups. These findings indicate that LPS-stimulated PGE2 release from peripheral blood monocytes may correlate with susceptibility to periodontitis in human subjects.
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PMID:LPS-elicited secretory responses in monocytes: altered release of PGE2 but not IL-1 beta in patients with adult periodontitis. 252 82


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