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)

Pathogenic bacteria constitute the primary extrinsic agent in the etiology of Adult periodontitis. In addition to direct toxic effects, bacteria induce destructive immunologic and other inflammatory reactions in the host, leading to the observed pathologic alteration in the tissue. The risk to develop periodontal disease is not equal for all individuals, suggesting host factors are important in determining an individuals disease susceptibility. Regulation of immune response is important in maintaining the equilibrium between periodontal health and disease. We hypothesize that, in the case of Adult periodontitis, a localized lack of the regulatory cytokine interleukin-4 (IL-4) in the gingival tissues predisposes susceptible individuals to progress from gingivitis to periodontitis.
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PMID:A localized absence of interleukin-4 triggers periodontal disease activity: a novel hypothesis. 149 19

Three serological markers of immune cell activation, interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R), and interleukin-4 (IL-4), were measured by enzyme-linked immunosorbent assays in 20 control subjects and 26 periodontitis patients. The experimental group comprised 19 juvenile/post-juvenile and 7 severe generalized periodontitis patients with radiographic evidence of alveolar bone loss. Although some control sera contained immunoreactive IL-2 (2 of 20) and IL-4 (3 of 20), all contained sIL-2R, the levels of which correlated well with age (r = 0.644). Mean levels of all three markers were significantly elevated in the sera of patients with periodontal disease compared to control values. However, there was a wide variation in the amounts detected; IL-2 (0.21-173.33 ng/ml); sIL-2R (217.95-1177.27 units/ml); IL-4 (3.17-16.35 pg/ml), which did not correlate with either the degree of bone loss or pocket formation observed clinically. Moreover, there was no correlation between the levels of IL-2, sIL-2R or IL-4 for any given individual in the experimental group. The finding that only 2 of the control sera contained IL-2 (10%) compared to 23 of the periodontitis patients (88.5%) suggests that, of the three parameters investigated, the measurement of IL-2 could provide a sensitive laboratory test for assessing periodontal disease activity. Nevertheless, a definitive study to determine the relationship of serum IL-2 levels to clinical parameters of disease activity will be necessary to confirm this observation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-2, interleukin-2 receptor and interleukin-4 levels are elevated in the sera of patients with periodontal disease. 183 52

Chronic periodontitis is characterized by dense infiltrations of B and T lymphocytes within the gingival connective tissue. Distinct anaerobic gram-negative bacteria as well as autoimmunity to collagen have been reported to play a role in the etiology and the pathogenesis of this disease. Here we describe the cloning and characterization of CD4+ and CD8+ T lymphocytes isolated from inflamed gingival tissue obtained from four patients with chronic periodontitis. Clones were raised with phytohemagglutinin and interleukin-2 and tested for proliferation in response to whole-cell antigens of Porphyromonas gingivalis, Prevotella intermedia, Actinobacillus actinomycetemcomitans, human collagen type I, and two bacterial heat shock proteins. CD4+ T-cell clones reactive with collagen type I were obtained from all four patients. Eighty percent of these clones had phenotypes resembling the mouse type 2 T helper (Th) phenotype, i.e., they produced high levels of interleukin-4 and low levels of gamma interferon. No collagen-type-I-reactive CD8+ clones were obtained. Bacterial-antigen-reactive CD4+ and/or CD8+ T-cell clones were also obtained from each patient, and the majority of the clones showed a Th0-like cytokine pattern and produced equal amounts of interleukin-4 and gamma interferon. Although most clones were reactive with P. intermedia, it seems that the immune response is not strictly directed against this particular microorganism, as clones reactive with one of the other bacteria were also obtained from two patients. We propose that collagen-specific CD4+ Th2-like T cells contribute to the chronicity of periodontitis but that their modes of activation might be controlled by Th0-like T cells specific for periodontitis-associated bacteria.
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PMID:Cloning, characterization, and antigen specificity of T-lymphocyte subsets extracted from gingival tissue of chronic adult periodontitis patients. 753 6

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

It has previously been reported that, in periodontitis lesions, T cells with a memory/activated phenotype and with a type 2 cytokine profile accumulate in an oligoclonal fashion. Delineation of the role of cytokines in periodontal inflammation has, however, been complicated because of cross-regulation and because of their overlapping and often redundant effects. The aim of this study was to examine messenger RNA levels for interferon gamma, interleukin 4 (IL-4), IL-10, IL-12 and IL-13 in gingival tissues and peripheral blood mononuclear cells of patients with adult periodontitis. Reverse transcription polymerase chain reaction and subsequent image analysis was used to determine the level of mRNA for each cytokine. The mean expression of interferon gamma mRNA was significantly higher in peripheral blood mononuclear cells than in gingival tissues. In contrast, the mean expression of IL-10 mRNA was higher in gingival tissues than in peripheral blood mononuclear cells. This high expression of IL-10 mRNA was, in fact, seen in only 7 gingival tissue samples with the majority of samples showing levels similar to peripheral blood mononuclear cells. There was no difference in the mean expression of IL-12 p35 mRNA between gingival tissues and peripheral blood mononuclear cells. However, IL-12 p40 mRNA was expressed higher in gingival tissues than in peripheral blood mononuclear cells in 6 out of 16 samples with significant difference of mean expression. Like IL-10, gingival tissue samples and peripheral blood mononuclear cells expressed similar levels of IL-12 p40 mRNA. There was no difference in the mean expression of IL-13 in gingival tissues and peripheral blood mononuclear cells. Nevertheless, more peripheral blood mononuclear cell samples demonstrated high IL-13 mRNA expression than gingival tissue samples. IL-4 mRNA was weak but detectable in 3 gingival tissue samples. These results support the concept that cytokines form complex networks in periodontitis lesions and that their overlapping and redundant effects should be taken into account when considering the pathology of inflammatory periodontal disease. Dichotomous expression of IL-10 and IL-12 p40 mRNA in the periodontal lesion may be associated with disease entity.
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PMID:Cytokine messenger RNA expression in chronic inflammatory periodontal disease. 946 81

To examine the role of T cell subgroups, Th1 and Th2, in the development of periodontitis, the expression of various cytokines was investigated in a mouse model of alveolar bone resorption using in situ hybridization (ISH) with digoxigenin-labeled oligonucleotides. When mice received repetitive injections with Escherichia coli lipopolysaccharide into the gingiva every 48 h, alveolar bone resorption was detectable after the fourth injection, reaching a maximum after the 13th injection. For the best performance of ISH, we first had to choose a decalcification protocol. Among various decalcification protocols, 10% EDTA (4 degrees C, 5-6 days) was the best for 28S rRNA staining. Positive cells for transcripts of interferon-gamma (Th1 product) were detected after the fourth injection, reaching a maximum after the tenth injection. A similar pattern was obtained for interleukin (IL)-10 mRNA (Th2 product) and IL-1beta, while the positive cell number reached a maximum after the 13th and 10th injections, respectively. The number of IL-4 mRNA (Th2 product)-positive cells remained low till the tenth injection, but increased thereafter. Consequently, we found that the population change from Th1 to Th2 in the inflammation site correlated with the transition from gingivitis to periodontitis, indicating differential roles of T cell subgroups in the development of periodontitis.
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PMID:Differential expression of IFN-gamma, IL-4, IL-10, and IL-1beta mRNAs in decalcified tissue sections of mouse lipopolysaccharide-induced periodontitis mandibles assessed by in situ hybridization. 956 83

Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.
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PMID:Inflammatory mediators of the terminal dentition in adult and early onset periodontitis. 968 17

The effects of Porphyromonas gingivalis stimulation on T-cell clonality and cytokine mRNA expression in peripheral blood mononuclear cells from individuals with gingivitis and periodontitis were investigated. Clonality of T cells was investigated by reverse transcription-polymerase chain reaction (RT-PCR) and single-strand conformation polymorphism analysis. Cytokine mRNA expression was investigated by RT-PCR. Whereas unstimulated mononuclear cells did not demonstrate obvious clonality, clonal expansion was found in most Vbeta families after stimulation. However, there was no relation between clonal change and disease category or the presence of P. gingivalis infection. Messenger RNA for interferon-gamma and interleukin-13 was upregulated whereas interleukin-4 and -10 were downregulated following P. gingivalis stimulation. Interleukin-12p35 demonstrated no consistent pattern. This study supports the concept that P. gingivalis stimulates T cells in an antigen-specific fashion. It further suggests that peripheral blood T cells may preferentially produce interferon-gamma and interleukin-13 in response to P. gingivalis stimulation irrespective of disease or P. gingivalis status.
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PMID:T-cell antigen specificity in humans following stimulation with Porphyromonas gingivalis. 1066 83

It has recently become apparent that the anti-heat shock protein (HSP) antibody plays an important role in the pathogenesis of atherosclerosis. We studied whether immunization with human HSP60 could lead to atherosclerosis in mice. We attempted to induce atherosclerosis in C57BL/6NJcl mice by immunization with human HSP60 under a high-cholesterol diet. The size of fatty streak lesions was significantly enhanced in mice immunized with human HSP60 under a high-cholesterol diet relative to the number in control mice receiving a high-cholesterol diet alone. In addition, these new atherosclerotic model mice showed lesions of inflammation in the periodontal tissue. This new model may thus provide theoretical support for the clinical observation that patients suffering from periodontitis are frequently found to have atherosclerosis. The cytokine ratio of interferon-gamma/interleukin-4 in the high-cholesterol diet group was significantly higher than that in the standard chow group (p<0.05). This suggests the presence of a predominantly Th1-type immune response in atherosclerosis.
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PMID:A new murine model for atherosclerosis with inflammation in the periodontal tissue induced by immunization with heat shock protein 60. 1101 2

To study mediators associated with the progression of disease and the process of bone regeneration in human apical periodontitis, we examined samples of periapical granulation tissues and regeneration tissues obtained from five patients by use of immunohistochemical methods. Periapical granulation tissues were found to contain a large number of CD4-positive T cells and CD68-positive monocytes/macrophages (CD4: 35.2%, CD68: 32.7%). The CD4-positive T cells and CD68-positive monocytes/macrophages were predominantly present in regeneration tissues (CD4: 62.1%, CD68: 16.0%). In these the percentages of CD4-positive T cells were higher as compared with periapical granulation tissues (from 35.2% to 62.1%). In periapical granulation tissues, CD4-positive T cells stained positively for interferon-gamma (IFN-gamma) and negatively for interleukin-4 (IL-4). In regeneration tissues, IL-4-producing cells could be detected. However, IFN-gamma-producing cells could not be detected. These results suggest that IFN-gamma and IL-4 may modulate the pathogenesis of infectious disease and the process of bone regeneration in local inflammation sites such as human apical periodontitis.
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PMID:Presence of IFN-gamma and IL-4 in human periapical granulation tissues and regeneration tissues. 1144 9


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