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)

Human gingival tissues from periodontitis patients were found to contain from 126 fg/mg to 2161 fg/mg interleukin-1 beta as determined by a sensitive enzyme linked immunoassay. No IL-1 beta could be found in normal gingival tissue. This finding may have important consequences relevant to connective tissue destruction and episodes of alveolar bone resorption characteristic of chronic periodontitis.
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PMID:Increased interleukin-1 beta (IL-1 beta) concentration in gingival tissue from periodontitis patients. 253 90

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

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

Interleukin-1 beta (IL-1 beta), a potent stimulator of bone resorption, has been implicated in the pathogenesis of periodontal destruction. However, the relationship between cytokines and periodontal disease has not been studied sufficiently to allow definitive conclusions. The aims of this study are to investigate crevicular IL-1 beta and the clinical status of patients with periodontitis and the effect of phase I periodontal therapy on levels of IL-1 beta. For this study, 130 gingival crevicular fluid (GCF) samples were harvested from non-inflamed (15) and diseased sites (115) in 11 patients with periodontitis. The gingival index (GI) and probing depth (PD) of each site was recorded initially and one month after treatment. The amount of IL-1 beta in the GCF was measured by enzyme-linked immunosorbent assay (ELISA) using an antibody specific for this cytokine. Before treatment, IL-1 beta was found in 12 of 15 non-inflamed gingival crevices and in 112 of 115 diseased pockets. The amount of IL-1 beta varied from 4.03 to 511.12 pg/site. The average amount of IL-1 beta from diseased sites was 3-fold greater than that from non-inflamed sites. Both total amount of IL-1 beta and the GCF volume, but not IL-1 beta concentration, were found to be correlated, positively, with GI score and PD. After therapy, 63 sites from 7 patients were re-examined, and the amount of IL-1 beta in 49 of 63 sites was found to have declined. These data suggest that the amount of crevicular IL-1 beta is closely associated with periodontal status. This relationship may be valuable in monitoring periodontal disease activity.
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PMID:Crevicular interleukin-1 beta in moderate and severe periodontitis patients and the effect of phase I periodontal treatment. 777 73

IL-4- and IL-6-producing cells in human periodontal disease tissues were investigated using immunohistochemical and in situ hybridization techniques. Immunohistochemical analysis demonstrated the presence of IL-4-producing cells within the CD45RO+ subset and the percentage of IL-4+ cells was significantly higher in periodontal lesions than in gingivitis tissues (p < 0.01). The percentage of IL-6-producing memory cells was higher in periodontal lesions compared with gingivitis tissues, although it was not statistically significant (p > 0.05). A reverse tendency in IL-4- and IL-6-positive cells was observed in a few individual cases. No IL-4 mRNA could be detected using the in situ hybridization technique. However, high levels of IL-6 mRNA were present in clinically healthy tissues, with a further increase in both epithelium and connective tissues affected by gingivitis, although only the former was significant (p < 0.025). There was a significant decrease in IL-6 mRNA in both the connective tissue (p < 0.025) and epithelium (p < 0.01) in periodontitis tissues compared with levels in gingivitis tissues. However, the levels of IL-6 mRNA in periodontal tissues were high compared with those of IL-1 mRNA, which was used in this study as a positive control. These results suggest that Th2-type cells may accumulate in periodontal lesions.
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PMID:IL-4- and IL-6-producing cells in human periodontal disease tissue. 781 73

One hundred and twenty-four gingival crevicular fluid (GCF) samples were harvested from 13 healthy and 111 diseased gingival sites in 10 patients with periodontitis. The total amount and concentration of interleukin-1 beta (IL-1 beta) in each sample was measured by the enzyme-linked immunosorbent assay (ELISA) technique using an ELISA Kit specific for this cytokine. The IL-1 beta was undetectable in 23% of the GCF from clinically non-inflamed sites (three out of 13), while it could mostly be identified in diseased sites (109/111). The amount of IL-1 beta varied from 4.03 to 511.12 pg/site in diseased GCF samples. The average IL-1 beta amount from diseased sites was three-fold that from non-inflamed sites. Total IL-1 beta amount and the GCF volume were significantly increased with elevated gingival index (GI) score and deeper probing depth (PD). However, no significant difference of crevicular IL-1 beta concentration (pg/microL) could be found among groups with different clinical parameters. Our results indicate that IL-1 beta was present in the GCF of most clinically non-inflamed gingiva and almost all diseased pockets. The significant elevation of total IL-1 beta amount and GCF volume in diseased sulci suggests that it is closely associated with the severity of periodontal disease.
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PMID:Increased interleukin-1 beta levels in gingival crevicular fluid of Chinese periodontal patients. 791 93

In this study, we sought to determine if human polymorphonuclear leukocytes (PMNs) derived from chronically inflamed tissues can produce inflammatory cytokines in vivo. Human gingival crevicular fluid (GCF) with adult periodontitis was collected, and PMNs in GCF were examined after purified by Ficoll-Hypaque gradient method. Cytokines from peripheral blood (PB) cells stimulated with concanavalin A, LPS, or zymosan were also characterized, since GCF contains predominantly PMNs (> 95%) with a small number of lymphocytes or macrophages. Production of interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumor necrosis factor-alpha (TNF alpha), and IL-6 in GCF or culture supernatants of peripheral blood cells was determined by ELISA. Significant levels of IL-1 alpha and IL-1 beta secretion were found in GCF. PB cells in culture showed prominent cytokine production from monocytes/macrophages, followed by lymphocytes. Human peripheral blood PMNs (PB-PMNs) also produced low levels of IL-1 alpha and IL-1 beta, but not TNF alpha and IL-6. These cells were also examined for cytokine mRNA expression using the reverse transcription-polymerase chain reaction analysis. Highly purified PMNs (> 99.5%) from GCF expressed mRNA for IL-1 alpha, IL-1 beta and TNF alpha, but not for IL-6. PB-PMNs in culture also showed mRNA expression for IL-1 alpha, IL-1 beta, and TNF alpha in a time- and dose-dependent manner, especially after stimulation with zymosan. Therefore, we concluded that human PMNs from inflamed tissues can produce IL-1 alpha, IL-1 beta, and TNF alpha in vivo, but not IL-6.
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PMID:Human polymorphonuclear leukocytes derived from chronically inflamed tissue express inflammatory cytokines in vivo. 802 49

We have shown that gamma delta T cells in human gingiva have an intraepithelial location and, that in the chronic inflammatory disease periodontitis, the expression of CD45RO and CD8 or CD4 is induced on gamma delta T cells. To study the role of gamma delta T cells in local antibacterial responses, we determined the cytokine profiles of isolated human gingival cells. Different T cell subpopulations, isolated by positive selection with mAb-coated magnetic beads and macrophages, as well as epithelial cells, were analyzed for expression of mRNA for 15 cytokines by reverse transcriptase-PCR. The ultrastructure of gingival gamma delta T cells was also studied. The gamma delta T cells expressed mRNA for IFN-gamma, TNF-alpha, TGF-beta 1, and IL-6. Expression of IFN-gamma was a consequence of inflammation. CD4+ gamma delta T cells expressed IFN-gamma only, whereas CD8+ gamma delta T cells expressed all four cytokines. CD8+ cells expressing IFN-gamma, TNF-alpha, and IL-6 in combination suggest a cytotoxic effector function. Gingival gamma delta T cells contained cytoplasmic electron-dense membrane-bound granules and multivesicular bodies that are ultrastructural characteristics of cytotoxic cells. Epithelial cells from inflamed gingiva expressed HLA-DR, CD1a, CD1c, and heat shock protein 60 on the cell surface. They also expressed mRNA for IL-1 beta, IL-6, IL-8, TNF-alpha, and TGF-beta 1. Thus, epithelial cells may function as accessory cells in immune activation and, at the same time, be target cells for CD8+ gamma delta T cells reactive with CD1 Ag or heat shock protein. These results suggest that gamma delta T cells constitute a first line of defense in gingiva, preventing entrance of pathogens by cytotoxicity against infected and stressed epithelial cells, and by control of epithelial cell growth through secretion of regulatory cytokines.
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PMID:Cytokine profile and ultrastructure of intraepithelial gamma delta T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. 805 26

Menopause and oophorectomy without estrogen therapy (ED) have been associated with increased production of bone-active cytokines by peripheral blood mononuclear cells. The current study extended evaluation to gingival crevicular fluid (GCF) levels of interleukin (IL)-1 beta and IL-6 in such subjects compared to premenopausal and postmenopausal estrogen-treated females (ES). 13 ED and 13 ES Caucasians with a history of moderate-severe adult periodontitis provided GCF from 1-3 clinically identical sites each (5-6 mm probing depth, 5-7 mm clinical attachment loss, bleeding on probing). 30 s GCF samples were obtained and evaluated for IL-1 beta and IL-6 levels using two-site enzyme-linked immunosorbent assays (ELISAs). The frequency of GCF IL-1 beta-positive subjects was elevated in ED versus ES (92% versus 23%; p < 0.0004, chi 2 analysis). IL-6 was detected more frequently in ED subjects (23% versus 8%; not significant); however, the frequency of IL-6 detection was low in both groups due to short sampling times. These data support the concept that clinical conditions causing low estrogen environments allow increased local production of the bone-active cytokine IL-1 beta, and perhaps IL-6.
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PMID:Gingival fluid IL-1 beta and IL-6 levels in menopause. 812 39

The secretion of prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF alpha), interleukin 1 beta (IL-1 beta), and interleukin 6 (IL-6) by adherent mononuclear cells (AMNC) from 28 patients with early-onset periodontitis was studied. The early onset-periodontitis patients consisted of 12 patients with localized juvenile periodontitis (LJP) and 16 patients with severe generalized periodontitis (SGP). The AMNC responses to different concentrations of lipopolysaccharide (LPS) (E. coli) were determined in these 28 patients and compared to 14 healthy controls. Mediator levels in the supernatant were measured using radioimmunoassays for PGE2, IL-1 beta, and IL-6 determination and an enzyme linked immunosorbent assay for TNF alpha levels. The mean age of the patients was 19.9 years for the LJP group, 30.4 years for SGP, and 28.0 years for the controls. The mean number of teeth per patient with attachment loss of > 6 mm was 4.75 in the LJP patients and 17.3 in the SGP group. In the absence of LPS, LJP AMNC secreted significantly more PGE2 than unstimulated control or SGP AMNC, while similar baseline amounts of IL-1 beta, IL-6, and TNF alpha were secreted by AMNC from the 3 patient groups. LPS stimulation resulted in the dose-dependent secretion of significantly higher levels of PGE2 by LJP AMNC compared to SGP AMNC which in turn secreted significantly more than controls. TNF alpha secretion by LJP monocytes was significantly greater than the SGP and the control groups while IL-1 beta secretion by the SGP AMNC was depressed compared to the other two patient groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The secretion of PGE2, IL-1 beta, IL-6, and TNF alpha by adherent mononuclear cells from early onset periodontitis patients. 815 10


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