UMLS:C0031099 - FACTA Search

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Query: UMLS:C0031099 (periodontitis)
12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IL-2, interferon-gamma (IFN-gamma), IL-4 and IL-6 producing T cells in periodontitis and gingivitis-affected human tissues were investigated by immunohistochemistry to clarify the relationship between T cell functional subsets and disease entity. Using alkaline-phosphatase anti-alkaline-phosphatase technique, the relative proportions of each cytokine-producing T cell were calculated in the crevicular 1/3, middle 1/3 and oral 1/3 areas selected in the connective tissue of sections. CD19:CD3 and CD4:CD8 ratios were determined on the serial sections. Compared with gingivitis tissues, the proportion of cytokine-producing cells in periodontitis-affected samples was higher overall in the crevicular 1/3 (P < 0.02). The middle 1/3 exhibited a higher percentage of cytokine-producing cells, except for IL-6-producing cells. Frequencies of cytokine-producing cells in the oral 1/3 did not differ. IL-4 was the prominent cytokine in periodontitis-affected tissues, with the highest proportion detected in the crevicular 1/3. The CD19:CD3 ratio was higher in periodontitis tissues irrespective of the location, indicating a B cell dominance in periodontitis lesions. Furthermore, a significant positive correlation between the proportion of IL-4-producing cells and the CD19:CD3 ratio was noted. The CD4:CD8 ratio consistently exceeded 2.0 in both periodontitis and gingivitis. These results suggest that immunoregulation of both periodontitis and gingivitis are T cell-dependent, but in periodontitis type 2 helper T cells predominate and thereby control B cell activation.
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PMID:Immunohistological analysis of T cell functional subsets in chronic inflammatory periodontal disease. 788 61

The purpose of this study was to compare, using cell blot analysis, the association of gingival tissue mononuclear cells (GTMC) isolated from lesions displaying histories of early-onset periodontitis (EOP; typically B-lymphocyte dominated) and gingivitis (typically T-lymphocyte dominated) with the B-cell stimulating cytokine, interleukin (IL)-4, and the T-cell stimulating cytokine, IL-2. Eleven EOP patients and 11 age- and gender-similar gingivitis control (GC) subjects participated. Gingival tissue adjacent to the alveolar crest normally removed during surgery was digested in collagenase-containing media and GTMC were isolated by density gradient centrifugation. Cells were separated into four aliquots. One was left unstimulated; the remainder were stimulated for 2 hours with Porphyromonas gingivalis outer membrane protein, mitogen Concanavalin A, or common antigen tetanus toxoid. Cells then were centrifuged onto transfer membranes and incubated in RPMI 1640 media for 6 hours to allow absorption of secreted cytokine. Membranes were treated with monoclonal anti-IL-2 or anti-IL-4, followed by a biotin-conjugated second layer, streptavidin-alkaline phosphatase and nitro blue tetrazolium/5-bromo-4-chloro-indolyl-phosphate (NBT/BCIP) color development. A higher percentage of GTMC from EOP patients were IL-2+ when stimulated with P. gingivalis compared with GTMC from GC patients (20 +/- 2% vs. 12 +/- 2%, P < 0.003). A higher percentage of non-stimulated GTMC from EOP patients produced IL-4 than from GC (22 +/- 4% vs. 6 +/- 3%, P < 0.00007), as well as when stimulated with P. gingivalis (22 +/- 3% vs. 13 +/- 2%, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gingival cell IL-2 and IL-4 in early-onset periodontitis. 799 15

Localized and chronically-inflamed gingival tissues of adult periodontitis (AP) are generally characterized as a hyper-responsiveness of B lineage cells where increased numbers of plasma cells occur. It was previously shown that high numbers of IgG subclass antibody-secreting cells (e.g., IgG1 > IgG2 > IgG3 > or = IgG4) with significant numbers of IgA subclass antibody-producing cells were seen in enzymatically dissociated gingival mononuclear cells (GMC) from inflamed periodontal tissues. An interesting finding was that the frequency of IgA2 plasma cells was elevated in the severe stage of AP when compared with the moderate stage. IgM plasma cells were essentially not found in these tissues. To understand the cytokine involvement in these increased B cell responses in inflamed gingiva, GMC isolated from inflamed tissues of AP patients were examined for cytokine production, specifically for IL-2, IL-4, IL-5, and IL-6 at both the protein and mRNA levels, since these cytokines have been shown to be essential interleukins for the regulation of the B cell response. Freshly-isolated GMC and peripheral blood mononuclear cells (PBMC) from AP patients were initially examined for IL-6 production because of its essential role for the terminal differentiation of B cells to become Ig-producing plasma cells. High levels of IL-6 were produced by GMC but not by PBMC unless cells were stimulated with T cell mitogen. A similar findings was also obtained when levels of IL-6 specific mRNA were examined in GMC and PBMC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokines and periodontal disease: immunopathological role of interleukins for B cell responses in chronic inflamed gingival tissues. 831 62

A unique characteristic of the localized inflammatory tissue in the periodontium (e.g., adult periodontitis [AP]) is the accumulation of IgG (IgG1 > IgG2 > IgG3 > or = IgG4) followed by IgA plasma cells (IgA1 > IgA2). However, the exact molecular mechanisms contributing to these elevated B-cell responses at the local disease site are still unknown. Thus, this study has examined the production of cytokines of importance in B-cell responses, e.g., interleukin (IL)-2, IL-4, IL-5, and IL-6 by gingival mononuclear cells (GMC) isolated from patients in severe stages of AP. These cytokines were assessed at the protein and messenger (m)RNA levels to understand their importance for the observed increased B-cell responses present in these tissues. Among the four cytokines tested by respective cytokine-specific, polymerase chain reaction and dot-blot hybridization, high levels of IL-5- and IL-6-specific mRNA were noted in GMC freshly isolated from AP patients. On the other hand, specific message for IL-2 and IL-4 were not present. Further, the analysis of culture supernatants of GMC also revealed that cells from AP patients spontaneously produced IL-5 and IL-6 but not IL-2 and IL-4. In contrast, when peripheral blood mononuclear cells isolated from the same patients were examined for these cytokines, no detectable levels of mRNA or secreted cytokines were noted. These results showed that GMC from localized inflammatory tissues in severe stages of AP possess a distinct cytokine profile represented by high levels of IL-5 and IL-6 mRNA expression and protein synthesis, whereas IL-2 and IL-4 were not detected. Further, this study supports the concept that AP is a localized inflammatory disease, because GMC from the inflamed tissue actively produce IL-5 and IL-6, whereas peripheral blood mononuclear cells from the same patients do not.
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PMID:Gingival mononuclear cells from chronic inflammatory periodontal tissues produce interleukin (IL)-5 and IL-6 but not IL-2 and IL-4. 847 96

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

Elevated numbers of plasma cells are associated with localized and chronically inflamed gingiva of patients with adult periodontitis. However, only limited information is currently available as to how cytokines produced by CD4(+) T cells are involved in these increased B cell responses in affected gingival tissues. When gingival mononuclear cells (GMC) were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4(+) T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4(+) T cells, RNA was extracted and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for interferon-gamma (IFN-gamma) and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13 (Th2) and beta-actin (internal control). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines, where one pattern was represented by expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the second consisted of mRNA for IFN-gamma, IL-6 and IL-13. In most samples, mRNA for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. When RNA was isolated from CD4(+) T cells of concanavalin A-stimulated peripheral blood mononuclear cells (PBMC) of the same patients and examined by RT-PCR, mRNA for all Th1 and Th2 cytokines were detected. These findings suggest that although human CD4(+) T cells are capable of producing an array of Th1- and Th2-type cytokines, the CD4(+) T cells associated with periodontitis are limited to production of IFN-gamma, IL-6, IL-13 and is some instances IL-10. CD4(+) T cells from diseased periodontal tissues are divisible into two groups based upon whether or not IL-10 is produced, together with IFN-gamma, IL-6 and IL-13.
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PMID:Selected Th1 and Th2 cytokine mRNA expression by CD4(+) T cells isolated from inflamed human gingival tissues. 860 41

Expression of mRNA for IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-5, IL-6 and TNF-alpha in inflamed gingiva was quantitatively examined by ribonuclease protection assay and in situ hybridization. The IL-1 beta mRNA expression level was statistically high (P < 0.05) in periodontitis-affected tissues compared with that in gingivitis-affected tissues. The densities of macrophages (identified as CD68-positive cells) and CD45RO-positive cells infiltrating in the inflamed gingiva correlated statistically with IL-1 beta transcript levels (macrophages, P < 0.001; CD45RO-positive cells, P < 0.002). In situ hybridization revealed IL-1 beta mRNA expression in infiltrating cells, presumed to be macrophages. The IL-1 alpha and IL-6 mRNA expression levels were much lower than the IL-1 beta transcript level, and mRNAs for IL-2, IL-4, IL-5 and TNF-alpha were negligible in these gingival tissues. The results indicate that IL-1 beta is a cytokine expressed predominantly in inflamed gingiva and reflects the density of infiltrating macrophages and other leukocytes.
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PMID:IL-1 beta mRNA as the predominant inflammatory cytokine transcript: correlation with inflammatory cell infiltration into human gingiva. 883 19

It has been suggested that the types of inflammatory round cell infiltrates and the divergence in the cytokine production profile by macrophages and helper T cells regulate the course of infectious or inflammatory diseases, including periodontitis and gingivitis. We examined the expression of IL-1alpha, IL-1beta, IL-2, IL-4, IL-5, IL-6 and tumour necrosis factor-alpha (TNF-alpha) mRNA in the inflamed gingiva by in situ hybridization. The results of single-cell analysis were used as data sets for statistical analyses. The density of cells expressing IL-1alpha, IL-4 and IL-5 mRNA was higher in periodontitis than in gingivitis. IL-2 mRNA-expressing cells were almost absent in gingivitis specimens. Principal component analysis disclosed three factors explaining 84.8% of the variance: one accounting for 40.5% of the variance and mainly regulated by IL-1alpha, IL-1beta, IL-6 and TNF-alpha, and two others, explaining 29.9% and 14.4% of the variance, describing the relationship between the types of cytokines derived from macrophages or Th2 type. These results suggest that the cytokines produced by inflammatory cells infiltrating in the gingival tissue are influential on the progression of gingivitis, an acute and reversible inflammatory condition, to chronic and destructive periodontitis. Thus, periodontal disease progression may be regulated by the local cytokine network, and the bias in this network towards a Th2-type cytokine dominance could be an exacerbating factor.
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PMID:Relevance of local Th2-type cytokine mRNA expression in immunocompetent infiltrates in inflamed gingival tissue to periodontal diseases. 901 Feb 72

An accumulation of elevated numbers of macrophages (M phi) and Ig producing cells is associated with localized and chronically inflamed gingiva of patients with adult periodontitis. When gingival lymphocytes were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4+ T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4+ T cells, RNA was extracted and reverse transcriptase polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for IFN-gamma and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13, (Th2) and beta-actin (housekeeping gene). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines. Thus, one pattern was represented by the expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the other case consisted of mRNA for IFN-gamma, IL-6, and IL-13. Except for a few cases, messages for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. The predominant expression of Th2 cytokines (e.g. IL-6, IL-10 and IL-13) may contribute to the induction of high B cell responses in local disease sites. On the other hand, lack of IL-4 may be responsible for the accumulation of M phi in diseased periodontium. We also investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and M phi persistence in the absence of exogenous IL-4. Gingival M phi, when compared with monocytes (MN)/M phi from peripheral blood mononuclear cells (PBMC), expressed high levels of IL-4R mRNA. When gingival M phi were incubated with recombinant IL-4 (rIL-4), the cell viability was dramatically reduced by apoptosis. These findings clearly show that the lack of IL-4 may contribute to the persistent occurrence of M phi at the disease site and addition of exogenous rIL-4 to gingival M phi cultures leads to cell death by apoptosis.
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PMID:Molecular and cellular mechanisms for periodontal diseases: role of Th1 and Th2 type cytokines in induction of mucosal inflammation. 908 20

In recent years advances in clinical techniques and procedures such as guided tissue regeneration and implants, have dominated periodontics. However, as we move towards the 21st century, emphasis is swinging 'back to basics' with the recognition that patient susceptibility to periodontal disease determines the ultimate outcome not only of the disease process but also of the treatment undertaken. In this context attention is returning to the host response and with the advent of clonal and molecular biological techniques, new insights are being gained into the nature of host susceptibility. Previous studies have suggested that a T-cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. More recently, T-cell subsets have been dichotomized on the basis of their cytokine profiles. In general, Th1 cells produce IL-2 and IFN-gamma while Th2 cells produce IL-4, IL-5 and IL-6. The major function of Th1 cells is to mediate delayed type hypersensitivity. In contrast the major function of Th2 cells is to provide B-cell help. A model for periodontal disease has now been developed based on this functional dichotomy which provides a framework for the study of cytokine profiles in periodontal disease. Early studies in this context have demonstrated higher proportions of IL-4 and IL-13 producing cells in periodontitis tissues together with possible variations in IL-10 production. Clonal studies have shown that the selection of a particular cytokine profile is not antigen dependent and that differences may be due to the host susceptibility although this remains to be determined.
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PMID:Periodontics into the 21st century. 917 77

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