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)

Mononuclear cell populations were studied in gingival biopsy specimens from adolescents (n = 10) with at least one periodontal pocket with an increased probing depth (greater than 5 mm). The marginal bone loss was measured on radiographs, subgingival plaque samples were collected from the lesions, and the microbial flora was identified. Specimens from gingivitis lesions (n = 5) were used as controls. The mononuclear cell populations in the specimens were detected by using monoclonal antibodies defining functional T-lymphocyte subpopulations, B lymphocytes, and monocytes. All gingival specimens from patients with increased probing depth showed large lymphocyte infiltrates, most of which were CD 3-antigen-positive cells (T lymphocytes). Few (2%) infiltrating T cells expressed receptors for interleukin-2. B cells were detected in most specimens from the periodontitis group and varied from less than 1% to 21%. This study indicates that lesions in adolescents with early signs of periodontitis are characterized predominantly by T-cell lesions with relatively few cell aggregates of B cells present.
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PMID:Subpopulations of lymphocytes in connective tissue from adolescents with periodontal disease. 169 57

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

Family case studies help us identify host risk factors in periodontal disease. In this study we examine a family consisting of a mother (40 years old, with rapidly progressive periodontitis), her elder daughter (14 years old, with localized juvenile periodontitis), and younger daughter (13 years old, with simple gingivitis). We examined 1) the peripheral neutrophil functions (chemotactic migration, phagocytosis, superoxide production); 2) lymphocyte functions (proliferative activity and cytokine productivity of T cells, immunoglobulin [Ig] M productivity of B cells when stimulated with pokeweed mitogen); 3) phenotypic analyses of peripheral lymphocyte subpopulations; 4) serum IgG antibody titers against periodontopathic bacteria; and 5) serological type of HLA class II. All the subjects exhibited high T4/T8 ratios due to high percentage of CD4-positive cells, showed high IgG titers to Actinobacillus actinomycetemcomitans, and had a HLA DQw1 in common. The mother showed a slight deficiency of neutrophil chemotactic migration to N-formyl methyonyl leucyl phenylalanin (fMLP), raised interleukin-2 productivity of T cell, and high levels of IgG titers to Porphyromonus gingivalis and Fusobacterium nucleatum. Both daughters showed weak T cell proliferative response to anti-CD3 monoclonal antibody and low IgM productivity. Low lymphocyte responsiveness may be involved in the pathogenesis of periodontal disease of these daughters; therefore, the lymphocyte dysfunctions shown should be considered in relation to the progression of periodontal disease.
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PMID:Host defensive functions in a family manifesting early-onset periodontitis. 870 71

In this cross-sectional study, we assessed the in vitro interleukin-2 (IL-2) producing capacity of peripheral blood mononuclear cells (PBMC) and lymphocytes from patients with different forms of periodontitis. 45 patients (12 with localised early onset periodontitis (LEOP), 20 with generalised early onset periodontitis (GEOP), and 13 with adult periodontitis (AP), and 20 periodontally healthy subjects (HS), participated in this study. PBMC and lymphocytes were isolated from the subjects and their cells were stimulated with an anti-CD3 monoclonal antibody (anti-CD3 MoAb) and the secreted IL-2 levels in the culture were bioassayed. No significant differences could be found in IL-2 producing activity of PBMC between the patients and HS group. There was wide interindividual variation and high and low "IL-2 producers" were noted. We found a LEOP patient who was a high producer of IL-2 (> mean + 8 SD) and 2 LEOP patients and a HS who were low producers of IL-2 (< mean - 1.5 SD) with their lymphocytes. Incidentally, the HS became a LEOP patient during 2 years after this study. The low IL-2 producing activity of their PBMC and lymphocytes against anti-CD3 MoAb could not be overcome by stimulation with phorbol myristate acetate and ionomycin. Thus, we found high and low IL-2 producing capacity by PBMC and lymphocytes in certain subjects and these subjects may be useful models in assessing the role of systemic IL-2 productivity associated with their progression of periodontal disease.
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PMID:Assessment of in vitro interleukin-2-producing capacity of peripheral blood lymphocytes from patients with periodontitis. 904 97

Virus-associated hemophagocytic syndrome (VAHS) is a disorder characterized by benign generalized histiocytic proliferation and marked hemophagocytosis associated with systemic viral infection. An immunodeficiency which includes an extremely decreased leukocyte and platelet count together with abnormalities in the CD4/CD8 ratio are the most common features of VAHS. Here we report an early-onset periodontitis (EOP) patient with VAHS from the standpoint of host-parasite interaction to understand the effect of this systemic disorder which might possibly influence susceptibility to periodontal disease. The patient is a 16-year-old Japanese male clinically diagnosed as having generalized EOP with slight gingival inflammation and moderate bone loss. This patient manifested VAHS at 3 years of age, and then had an unusual 4 recurrences (at 5, 7, 11, and 14 years old). Laboratory tests conducted include: 1) complete blood analyses: 2) peripheral neutrophil functions (chemotaxis, phagocytosis, superoxide production, and adherence); 3) peripheral lymphocyte subpopulations and functions, T-cell proliferative activity and productivity of cytokines (interleukin-2 [IL-2], interferon gamma [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]); 4) serum cytokine levels (IL-1 beta, IL-2, soluble IL-2 receptor [sIL-2R], IL-4, IL-6, IFN-gamma, and TNF-alpha; 5) serum immunoglobulin G (IgG) antibody titers against periodontopathic bacteria; 6) serological human leukocyte antigen (HLA) typing; and 7) determination of bacterial flora of the periodontal pockets. The results indicated that the patient's neutrophil chemotaxis and random migration were below the normal range. In lymphocyte examinations, T-cell proliferative activity, IL-2, and IFN-gamma productivity were elevated. Serum IFN-gamma level was also significantly higher than normal range. No specific periodontopathic bacteria were predominant in the periodontal pockets, however, the serum IgG titer against Porphyromonas gingivalis was elevated throughout the examination period. It is suggested that VAHS might be a possible risk factor for periodontal disease, and hence may serve as a model in understanding the role of host defense mechanisms in the establishment of inflammatory periodontal disease.
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PMID:Host defensive, immunological, and microbiological observations of an early-onset periodontitis patient with virus-associated hemophagocytic syndrome. 944 99

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

Porphyromonas gingivalis, a gram-negative, black-pigmented anaerobe, is among the microorganisms implicated in the etiology of adult periodontal disease. This bacterium possesses a number of factors, including hemagglutinins, of potential importance in virulence. Several hemagglutinin genes have been identified, cloned, and expressed in Escherichia coli. The purpose of this study was to characterize host responses to purified recombinant hemagglutinin B (rHag B), using the conventional Fischer rat as the experimental animal model. The effectiveness of immunization with rHag B on protection against experimental periodontal bone loss following infection with P. gingivalis was also evaluated. Groups of rats were immunized by the subcutaneous route with rHag B in complete Freund's adjuvant, immunized with rHag B and orally infected with P. gingivalis, nonimmunized and noninfected, or orally infected with P. gingivalis only. Serum and saliva samples were collected throughout the experiment and evaluated for serum immunoglobulin G (IgG) and IgM and salivary IgA antibody activity by enzyme-linked immunosorbent assay. No salivary IgA anti-Hag B activity was detected in the various groups of rats. A slight serum IgM response similar to that seen in preimmune samples was observed. Serum IgG antibody activity to Hag B was detected only in samples from rats immunized with rHag B. This response was primarily of the IgG1 and IgG2a subclasses, followed by IgG2b and low levels of IgG2c. Supernatants from rHag B-stimulated splenic lymphoid cell cultures from immunized rats contained high levels of gamma interferon, followed by interleukin-2 (IL-2), IL-10, and then IL-4. These results are consistent with the induction of T helper type 1 (Th1)- and Th2-like responses. Western blot analysis of sera derived from rHag B-immunized rats reacted with trichloroacetic acid (TCA) precipitates of P. gingivalis 33277, 381, A7A1-28, and W50, revealing a 50-kDa band reflective of Hag B. However, sera derived from rats immunized with P. gingivalis whole cells or from rats infected with P. gingivalis only did not react with rHag B but did react with TCA precipitates of P. gingivalis strains. Finally, radiographic measurements of periodontal bone loss indicated that rats immunized with rHag B had less bone loss than those infected with P. gingivalis only. These results demonstrate the effectiveness of purified rHag B in inducing a protective immune response and support the potential usefulness of this component of P. gingivalis in the development of a vaccine against adult periodontitis.
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PMID:Host responses to recombinant hemagglutinin B of Porphyromonas gingivalis in an experimental rat model. 1045 74

The purpose of our study was to investigate the immune response in chronical periapical parodontitis (CPP) by using multidisciplinary approach. 30 CPP samples were obtained after surgical removal--apicoectomy. Each CPP sample was examined by histological, bacteriological and flow cytometrical (FC) analysis of lymphocytes infiltrating CPP samples. Ten percent of bacteriological samples were sterile, others had significant aerobic and anaerobic growth. We used pathohistologic and microbiologic findings and compared them to the results of immunological analysis. By FC we found a significant increase in proportions of T lymphocytes expressing interleukin-2 receptors and ICAM-1 compared to peripheral blood lymphocytes. Proportions of T helper cells that produce interferon-gama (IFN-gamma) was higher in CPP samples predominantly colonized by anaerobic bacteria. There were no differences in IL-4 expression by T cells in both groups (anaerobic and streptococcal). Among anaerobic CPP samples differences in proportion of T cells that express IL-2 receptors expression was also found between samples colonised by P. acnes and Bacteroides sp. Oral streptococci cause relatively limited tissue destruction and induce Th2 type of immune response accompanied by non-cytotoxic inflammatory reaction. On the contrary, anaerobic bacteria induce Th1 type of immune response that cause more severe inflammatory reaction (type 4) of hypersensitivity that damage the tissue by the action of cytotoxic T cell activation.
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PMID:Immune response in chronic periapical parodonititis. 1100 23

The tissue destruction seen in chronic periodontitis is commonly accepted to involve extensive upregulation of the host inflammatory response. Protease-activated receptor 2 (PAR-2)-null mice infected with Porphyromonas gingivalis did not display periodontal bone resorption in contrast to wild-type-infected and PAR-1-null-infected mice. Histological examination of tissues confirmed the lowered bone resorption in PAR-2-null mice and identified a substantial decrease in mast cells infiltrating the periodontal tissues of these mice. T cells from P. gingivalis-infected or immunized PAR-2-null mice proliferated less in response to antigen than those from wild-type animals. CD90 (Thy1.2) expression on CD4(+) and CD8(+) T-cell-receptor beta (TCRbeta) T cells was significantly (P < 0.001) decreased in antigen-immunized PAR-2-null mice compared to sham-immunized PAR-2-null mice; this was not observed in wild-type controls. T cells from infected or antigen-immunized PAR-2-null mice had a significantly different Th1/inflammatory cytokine profile from wild-type cells: in particular, gamma interferon, interleukins (interleukin-2, -3, and -17), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha demonstrated lower expression than wild-type controls. The absence of PAR-2 therefore appears to substantially decrease T-cell activation and the Th1/inflammatory response. Regulation of such proinflammatory mechanisms in T cells and mast cells by PAR-2 suggests a pivotal role in the pathogenesis of the disease.
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PMID:Protease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis. 1993 35


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