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)

Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post-active treatment clinical attachment loss (> 2% sites/year lost > or = 3 mm) were compared to 10 age-, race-, and supragingival plaque-matched patients with low post-treatment clinical attachment loss (< 0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL-1 alpha, IL-1 beta, IL-6) as determined by two-site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patient produced significantly more IL-6 (30.1 +/- 4.0 versus 15.4 +/- 2.8 nM, p < 0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL-1 concentrations. These data suggest that gingival IL-1 and IL-6 production is different in response to local and systemic factors associated with periodontitis, and that IL-6 may play a role in the identification and mechanisms of refractory periodontitis.
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PMID:Gingival fluid IL-1 and IL-6 levels in refractory periodontitis. 838 8

Ligature-induced periodontitis was monitored for 6 months in eight Macaca mulatta monkeys to examine clinical status, radiographic bone level, and crevicular fluid (CF) levels of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha, and leukotriene B4 (LTB4). A split-mouth design was used, with eight ligated teeth and eight contralateral nonligated teeth which develop soft-chow-promoted (spontaneous) disease. Ligated sites experienced an average attachment loss of 0.94 mm per site and linear bone loss of 0.88 mm per site, with spontaneous-periodontitis sites experiencing approximately half the loss of ligated sites. The CF mediator levels showed increased levels of PGE2 and TxB2 at the ligated sites, as compared with the spontaneous sites, with no significant contralateral differences in the IL-1 beta or LTB4 responses. The concentrations of LTB4 in CF reached an early threefold peak over the baseline level at 1 month. By 2 months there was a statistically significant threefold elevation in CF-PGE2 in the ligated sites and a twofold elevation in the spontaneous sites as compared to the baseline level (P = 0.041 and 0.008, respectively). The monocyte product IL-1 beta increased sharply at 2 months and returned to the baseline level by 6 months at both ligated and nonligated sites. Tumor necrosis factor alpha in CF was below the limit of detection at all sites throughout the experiment (i.e., < 2 ng/ml). The selective elevation of both PGE2 and TxB2 in ligated sites, compared with levels in spontaneous sites, in the presence of similar levels of LTB4 and IL-1 beta provides further evidence that these molecules regulate the magnitude of the tissue-destructive response in progressive periodontitis.
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PMID:Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey. 838 62

Interleukin-1 beta (IL-1 beta) and the four IgG subclasses were measured in gingival crevicular fluid (GCF) at 35 sites in 19 patients with adult periodontitis. Serum concentrations of the IgG subclasses were assayed in 16 patients. IL-1 beta was detected in GCF at 88.6% of sites at concentrations ranging from 12.38-420.90 pg/microliters (mean 138.35 +/- 112.61 pg/microliters). IgG1 was detected at 81.2% sites, IgG2 at 93.6%, IgG3 at 71% and IgG4 at 71%. Absolute concentrations in GCF were: IgG1--2.419 g/l +/- (SD) 3.389; IgG2--2.945 +/- 6.434; IgG3--0.118 +/- 0.144; IgG4 0.864 +/- 1.336. There were no significant correlations between IL-1 beta concentrations, GCF volume or the clinical status of the sample site. IL-1 beta was not correlated with any of the IgG subclasses. The absolute concentrations of all subclasses in GCF were significantly negatively correlated with GCF volume and positively correlated with the Bleeding Index. Only IgG4 was significantly negatively correlated with the probeable crevice depth index. The concentration of each IgG subclass was positively correlated with the other three IgG subclasses. Subclass concentrations in GCF, relative to serum concentrations, were not correlated with GCF volume or clinical status. Relative concentrations of IgG1, IgG2 and IgG3 showed significant positive correlation with each absolute concentration of the other subclasses but IgG4 did not show this relation. It was concluded that IL-1 beta is not related to clinical measurements of inflammation or previous attachment loss. The data suggest that IgG in GCF is largely derived from plasma but that some IgG4 may be locally synthesized.
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PMID:Interleukin-1 beta and IgG subclass concentrations in gingival crevicular fluid from patients with adult periodontitis. 844 21

The purpose of this investigation was to evaluate lipopolysaccharide (LPS)-stimulated monocyte secretory responses longitudinally in patients with generalized severe chronic adult periodontitis (periodontitis-susceptible) and controls with gingivitis (periodontitis-resistant). In addition, the expression of constitutive (Leu-M3) and LPS-inducible (Mo3e) antigens on monocytes isolated from these two groups was examined. Monocyte secretory function was assessed longitudinally; the effect of periodontal therapy in the susceptible patients was examined by comparing monocyte function before and after their treatment. Peripheral blood monocytes were isolated by counterflow centrifugal elutriation and treated with control medium or media containing 1 microgram/ml of Salmonella typhimurium LPS or Prevotella intermedia LPS with or without human recombinant interferon (IFN)-gamma pretreatment. Prostaglandin E2, F2 alpha and thromboxane B2 were quantified in culture samples by gas chromatography-mass spectrometry (GC-MS) and interleukin-1 beta was quantified by enzyme-linked immunosorbent assay. Leu-M3 and Mo3e antigen expression was assessed by FACScan. Three major findings were made. First, LPS-stimulated IL-1 beta release by monocytes from susceptible patients was depressed relative to that in resistant patients at the initial donation. After periodontal therapy, there was virtually identical IL-1 beta release in LPS-stimulated cultures from both groups. However, in susceptible patients IL-beta release was diminished after periodontal therapy in cultures pretreated with IFN-gamma. Second, there was a significant drift in monocyte secretion of prostaglandin E2 in samples from the resistant patients between the first two donations and the third donation. PGE2 release did not differ between groups at the initial donation, although there was a depression in PGE2 release in the susceptible group at the final donation when IFN-gamma was followed by S. typhimurium LPS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal evaluation of peripheral blood monocyte secretory function in periodontitis-resistant and periodontitis-susceptible patients. 851 3

Interleukin-1 beta (IL-1 beta) mRNA-expressing cells in human gingival crevicular washings (GCW) obtained from patients with periodontitis and healthy controls were examined by in situ hybridization. GCW was done at 15 diseased sites [Gingival Index > 1; pocket depth > or = 5 mm] from five patients with adult periodontitis and eight clinically periodontal healthy sites from three volunteers GI < or = 1; PD < or = 3 mm), and then the samples were cytocentrifuged. In situ hybridization using digoxigenin-labelled oligonucleotide probe complementary to human IL-1 beta mRNA showed IL-1 transcripts in both polymorphonuclear leucocytes and mononuclear cells but not in epithelial cells in all GCW samples from diseased and healthy sites. Polymorphs were the predominant leucocytes in diseased and healthy sites, averaging 91.7 +/- 4.6 and 77.0 +/- 10.3%, respectively. The percentages of IL-1 beta mRNA-positive polymorphonuclear leucocytes in GCW samples from diseased and healthy sites were 92.3 +/- 4.7 and 80.9 +/- 10.3%, respectively. The IL-1 beta gene signals in individual cells were quantified in five samples (two healthy and three diseased sites). The mean amounts of IL-1 beta mRNA expression in polymorphonuclear leucocytes was higher than that of mononuclear cells in all samples and there was heterogeneity within the populations of polymorphonuclear and mononuclears cells in their ability to express the IL-1 beta gene. These findings indicate that IL-1 beta may be predominantly produced by polymorphonuclear leucocytes in the gingival crevice of patients with adult periodontitis and periodontally healthy controls.
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PMID:Detection of interleukin-1 beta mRNA-expressing cells in human gingival crevicular fluid by in situ hybridization. 852 4

Recent in vitro findings indicate that cytokines represent an important pathway of connective tissue destruction in human periodontitis. The biological effects of interleukin-1 beta (IL-1 beta) and interleukin-8 (IL-8) are relevant in this regard, and the objective of this study was to compare the levels of these molecules in gingival crevicular fluids (GCF) from patients with adult periodontitis (experimental group) and from individuals with clinically healthy gingiva (control group). GCF was collected for 30 seconds using a periopaper strip and the volume of the sample determined. Following elution of the fluid, assays for IL-1 beta and IL-8 were carried out by ELISA. The concentrations (ng/ml) of cytokines were calculated in the original volume of GCF on each strip. The total amounts (pg/site) of cytokines were expressed as the concentrations multiplied by volumes of GCF: The total amounts of IL-1 beta and IL-8 of the experimental group were significantly higher than the control group. The total amounts of both cytokines were markedly reduced following phase 1 periodontal treatment. The clinical parameters were positively related to the total amounts of IL-1 beta and IL-8. IL-1 beta concentrations and total amounts were also positively related to IL-8 suggesting that the GCF IL-8 levels are influenced by local IL-1 beta activities. These data indicate that the total amounts of IL-1 beta and IL-8 exhibited dynamic changes upon severity of periodontal disease. The levels of IL-1 beta and IL-8 in GCF are valuable in detecting the inflammation of periodontal tissue.
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PMID:Levels of interleukin-1 beta and interleukin-8 in gingival crevicular fluids in adult periodontitis. 853 67

Refractory periodontitis manifests as a rapid, unrelenting, progressive loss of attachment despite the type and frequency of therapy. This study examined possible relationships between cytokine levels in gingival crevicular fluid (GCF), occurrence of specific periodontopathic microflora, and disease activity in patients with refractory periodontitis. Refractory periodontitis patients (7 male and 3 female) were selected on the basis of history and longitudinal clinical observations. In each patient, 2 teeth with pocket depths greater than 6 mm were selected and individual acrylic stents were fabricated with reference grooves for each site. The sites were examined at both baseline and 3 months later. The pattern and amount of alveolar bone resorption were assayed by quantitative digital subtraction radiography. Pocket depth and attachment loss were measured with a Florida Probe. The gingival index was measured at 4 sites around each sample tooth. Sites were divided into active sites (> or = 2.1 mm loss of attachment in 3 months) or inactive sites (< or = 2.0 mm loss of attachment in 3 months). The distribution and prevalence of the predominant microflora in active and inactive sites were compared using anaerobic culture and indirect immunofluorescence. Interleukin-1 beta, 2, 4, 6 and tumor necrosis factor-alpha (TNF-alpha) levels in gingival crevicular fluid (GCF) were quantified by ELISA. Prevotella intermedia and Eikenella corrodens significantly decreased in inactive sites but remained the same in active sites after 3 months. The active sites revealed significantly higher GCF levels of IL-2 and IL-6 than inactive sites at both baseline and at 3 months. IL-1 beta was also significantly greater in active sites than in inactive sites at 3 months. Alveolar bone loss in active sites correlated with increased GCF levels of IL-1 beta and IL-2. These results suggest that GCF levels of IL-1 beta, IL-2 and IL-6 and P. intermedia and E. corrodens in subgingival plaque may serve as possible indicators of disease activity in refractory periodontitis.
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PMID:The subgingival microflora and gingival crevicular fluid cytokines in refractory periodontitis. 855 Aug 66

The bone-resorptive cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have been implicated in the pathogenesis of many chronic inflammatory diseases, including pulpitis and apical periodontitis.To further elucidate their role in these disorders, we have identified cells that express IL-1 alpha and TNF alpha in infected pulps and in developing rat periapical lesions after surgical pulp exposure. As detected by immunohistochemistry, IL-1 alpha- and TNF alpha-positive cells were present as early as 2 days after pulp exposure in both the pulp and periapical region. The numbers of cytokine-expressing cells increased up to day 4 in the pulp and up to day 30 in the periapex. In contrast, cells expressing IL-1 beta and TNF beta, the homologous forms of these mediators, were not found in pulp or periapical lesions during this period. Cells expressing IL-1 alpha and TNF alpha were identified primarily as macrophages and fibroblasts, with occasional staining of polymorphonuclear leukocytes. Osteoblasts and osteoclasts were also positive, whereas lymphocytes were negative. In general, cytokine-expressing cells were located proximal to abscesses and the root apex. These findings demonstrate that cells that express bone-resorptive cytokines IL-1 alpha and TNF alpha are present immediately after pulp exposure in this model, which supports the hypothesis that these mediators play a key role in pulpal and periapical pathogenesis, including the concomitant bone destruction. They also indicate that both resident connective tissue cells as well as infiltrating cells express bone-resorptive cytokines in response to infection in these lesions.
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PMID:Immunolocalization of bone-resorptive cytokines in rat pulp and periapical lesions following surgical pulp exposure. 860 33

Alveolar bone-derived polymorphonuclear leukocytes (PMNs) were characterized for their ability to produce inflammatory cytokines such as interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumor necrosis factor alpha (TNF alpha), and IL-6 in vivo. Periapical exudates (PE) were collected from periapical lesions with chronic periapical periodontitis through root canals. Cells and noncellular supernatants were then isolated by centrifugation. The concentration of cytokines present in the noncellular supernatants were determined by ELISA. High concentrations of IL-1 alpha, IL-1 beta, and IL-6 were detected in PE, however, TNF alpha was not. PE contains predominantly PMNs ( > 95% of residing cells) with a few percent of lymphocytes and/or macrophages. These alveolar bone-derived PMNs were purified by the Ficoll-Hypaque gradient method and were analyzed for cytokine mRNA expression using the cytokine-specific reverse-transcription polymerase chain reaction. Highly purified PMNs ( > 99.5%) isolated from PE expressed significant levels of mRNA for IL-alpha, IL-1 beta, and TNF alpha. IL-6 mRNA was not detected, although a high concentration of IL-6 was detected in supernatants of PE by ELISA. The IL-6 secretion in PE could be derived from macrophages, T lymphocytes, osteoblasts, or fibroblasts around periapical lesions. These data strongly suggest that human PMNs derived from alveolar bone can spontaneously produce IL-1 alpha, IL-1 beta, and TNF alpha at sites of inflammation, and probably initiate inflammation and regulate augmentation of bone resorption in vivo.
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PMID:Expression of inflammatory cytokine genes in vivo by human alveolar bone-derived polymorphonuclear leukocytes isolated from chronically inflamed sites of bone resorption. 866 55

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking-related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone-resorbing factors, PGE2 and IL-1 beta. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non-smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 ng/ml, 1 microgram/ml, 10 micrograms/ml and 100 micrograms/ml) with or without 10 micrograms/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE2 and IL-1 beta by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE2 and IL-1 beta above that of unstimulated cultures. However, PGE2 release was potentiated 1.7-fold by the combination of P. gingivalis LPS and 10 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.05, one-way ANOVA). Prostaglandin E2 release also was potentiated 3.5-fold by P. gingivalis LPS and 100 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.00001, one-way ANOVA) and 3.1-fold by E. coli LPS and 100 micrograms/ml nicotine relative to E. coli LPS alone (p < 0.00001, one-way ANOVA). IL-1 beta secretion was lower for either LPS plus 100 micrograms/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS-mediated monocyte secretion of PGE2 by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.
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PMID:Nicotine effects on PGE2 and IL-1 beta release by LPS-treated human monocytes. 870 46


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