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)

The influence of pentoxifylline on normal and diseased neutrophil function has been studied in vitro. In high concentrations pentoxifylline stimulated human neutrophil chemotaxis toward both bacterial oligopeptides and complement components. Pentoxifylline was also shown in vitro to restore the normal chemotactic capacity of neutrophils from patients with known functional defects, i.e. myelodysplastic syndromes, lazy leucocyte syndrome, juvenile parodontitis, hyper-IgE-syndrome and liver cirrhosis. Pentoxifylline was also shown to strongly inhibit the release of primary and secondary granule release of granulocytes. Moreover, pentoxifylline inhibits both basal and stimulated neutrophil adhesion to both aortic and pulmonary artery calf endothelium. The mechanism whereby pentoxifylline exerts this action is not adequately understood. While our results partially imply interference of pentoxifylline with neutrophil cyclic AMP and/or prostaglandin metabolism, down-regulation of neutrophil functional antigen (e.g. CD11, CD18) expression seems to play a key role in the observed drug effects. Finally, these results indicate that pentoxifylline may be useful in the treatment of granulocyte mediated diseases and symptoms.
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PMID:In vitro modulation of normal and diseased human neutrophil function by pentoxifylline. 197 92

Human systemic antibody levels to oral members of the Bacteroides genus were assessed with an enzyme-linked immunosorbent assay. Antibody levels to B. gingivalis, two homology groups of B. intermedius, B. melaninogenicus, B. denticola, B. loescheii, B. corporis, B. oralis, B. buccae, and B. gracilis were determined in subjects with localized juvenile periodontitis, advanced destructive periodontitis, or adult periodontitis and in normal persons. Significantly elevated serum immunoglobulin G (IgG) antibody levels to B. gingivalis were seen in adult and advanced destructive periodontitis patients. Serum IgM and IgA antibodies were increased in diseased versus normal subjects, whereas negligible levels of serum IgE antibody were detected to this microorganism. Serum IgG antibody levels to B. intermedius were increased in advanced destructive periodontitis patients; however, the frequency of elevated responses were similar among the groups. Extreme antibody levels to the other Bacteroides spp. were occasionally observed in this population. Additionally, all of the elevated levels were found in diseased patients. Distribution analyses of the antibody levels indicated that most patients exhibited a pattern of elevated antibodies to a limited number of the oral Bacteroides spp. The results suggested that elevated systemic antibody levels to oral Bacteroides spp. are more frequently found in periodontal disease patients. These antibody responses presumably reflect a colonization of the patients. The distribution of the responses may indicate the potential pathogenicity of the microorganisms and is consistent with distinctive host-parasite interactions in this disease.
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PMID:Human immune responses to oral microorganisms: patterns of systemic antibody levels to Bacteroides species. 394

Local immunologic responses were studied in eleven patients with periodontitis, ten patients with juvenile periodontitis, and ten control subjects by performing immunofluorescence on gingival biopsies. F(ab')2 monospecific conjugates to human IgG, IgM, IgA, IgD, and kappa and lambda light chains were used as well as monospecific conjugates to human IgE and properdin. Biopsies from patients with juvenile periodontitis displayed a more intensified immunologic response as evidenced by increases of (I) positive cells stained with a F(ab')2 antihuman immunoglobulin conjugate; (2) IgG, IgM, and kappa and lambda containing cells; (3) extracellular fluorescence of IgG, IgM, IgA, and kappa and lambda light chains; and (4) properdin deposition. Neither IgD nor IgE conjugates reacted significantly with biopsies from the three patient groups. These findings support our previous conclusion that immunologic responses in periodontitis and juvenile periodontitis appear qualitatively similar, but that patients with juvenile periodontitis exhibit a more intense immune response.
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PMID:Immunopathology of periodontal disease. II. Immunofluorescent studies on the localized immune response in periodontitis and juvenile periodontitis. 617 7

In the present study the concentrations of IgE and histamine were determined in gingival tissue of patients with asthma (N = 15), patients with periodontitis (N = 21) and healthy controls (N = 18). Gingival IgE concentrations in the asthma group were markedly elevated confirming the results obtained in previous studies on salivary IgE concentrations. An increase of IgE was also observed in the periodontitis group. Histamine concentrations in the asthma group did not differ from the healthy controls, while in the periodontitis group a significant decrease in gingival histamine concentrations was found.
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PMID:Gingival IgE and histamine concentrations in patients with asthma and in patients with periodontitis. 658 12

Humoral responses were examined in idiopathic juvenile periodontitis (IJP) including antibody titers to representative strains of the five groups of periodontosis-associated bacteria. Titers as determined by indirect immunofluorescence were compared in IJP, non-IJP family members, periodontitis and periodontally healthy subjects. Serum concentrations of IgG, IgA, IgM and IgE were also assayed. Antibody titers to the periodontosis-associated bacteria were generally low. Some disease specificity was observed in that titers to Groups II and III bacteria were highest in IJP. These titers in IJP were significantly higher (P less than 0.01) than in the other subjects. Titers to Group I bacteria were similar in all periodontal groups except the periodontally healthy subjects where titers were the lowest. Titers to Group I bacteria were significantly higher (P less than 0.01) than in the periodontally healthy subjects. Titers to Groups IV and V were uniformly low in all periodontal groups. Immunoglobulin concentrations of IgA, IgM and IGE were similar in IJP and non-IJP. The IgG concentrations in IJP, while within the normal range were significantly higher in IJP compared to non-IJP family members.
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PMID:Humoral immunologic responses in idiopathic juvenile periodontitis (periodontosis). 692 68

To study the salivary response in asthma and periodontitis, calcium and phosphorus concentrations were determined from parotid and whole saliva. The IgE and histamine concentrations and the activities of lysozyme and arginine aminopeptidases were assayed from whole saliva. The values were compared with those obtained from matched healthy controls (n = 20 in each group). In whole saliva the phosphorus concentrations were elevated in the asthma group and the calcium concentrations in the periodontitis group. Regarding parotid saliva no significant differences between the groups were observed. The results indicate that in patients with asthma the IgE concentrations in whole saliva were elevated, while in patients with periodontitis and in healthy controls no detectable values were obtained. Both histamine and lysozyme concentrations seemed to increase in the asthma and periodontitis groups. A slight increase was also observed in the arginine aminopeptidase activities in the saliva of patients with asthma and patients with periodontitis.
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PMID:Studies of immunologic and inflammatory factors in saliva in patients with asthma and in patients with periodontitis. 694 23

Our previous studies showed that the expression of CD23 on polymorphonuclear leukocytes (PMNLs) in gingival crevicular fluid (GCF) from adult periodontitis (AP) patients was higher than in autologous peripheral blood (PB). Percentages of eosinophils in GCF PMNLs ranged between 6 and 14%. The purpose of the present studies was to increase understanding of the potential role of eosinophils and their products, including CD23, in periodontal disease. We analysed the eosinophil fraction in GCF and PB by flow cytometry using monoclonal antibodies to CD23b (BB10), eosinophil cationic protein (ECP) in stored and secretory forms (EG1 and EG2), and CD67 (80H3). Simultaneously, we measured IgE and soluble CD23 titer and GCF and serum by ELISA. Flow cytometric analysis of BB10, EG2 and 80H3 binding showed that GCF eosinophils from AP were activated. A large BB10+ EG2+ cellular fraction was detected in GCF from AP whereas it was very low in autologous serum (9.30 +/- 2.460 vs 0.16 +/- 0.10, p < 0.001). GCF from gingivitis patients exhibited no flow cytometric evidence for the presence of BB10+ EG2+ cells. BB10+ EG1+ cells, or inactivated eosinophils rated lower in GCF than in PB both in gingivitis and periodontitis patients (0.45 +/- 0.63 vs 1.83 +/- 0.96 and 0.15 +/- 0.30 vs 1.30 +/- 0.20, p < 0.05, respectively). IgE titer in AP patients reached 1208.1 +/- 421.2 IU/ml in GCF while only 49.1 +/- 50.4 in sera. Soluble CD23 in GCF reached 236.1 +/- 81.3 ng/ml in GCF and 5.6 +/- 1.8 ng/ml in sera. GCF of gingivitis patients, however, contained no detectable sCD23.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presence of activated eosinophils, high IgE and sCD23 titers in gingival crevicular fluid of patients with adult periodontitis. 747 97

Sixty-three dental periapical lesions were investigated in order to study the involvement of inflammatory and immunologic reactions in the pathogenesis and maintenance of chronic apical periodontitis. Of 61 well-preserved specimens, 38 were classified as granulomatous, 3 as exudative periapical granulomas and 20 as periapical scars. The quantitative composition of T-lymphocyte subpopulation and macrophages, the proportion of IgE-producing cells compared with other immunoglobulin producing plasma cells, and the tissue distribution of IgE-producing plasma cells compared with that of mast cells were determined in the granulomatous types of granulomas using immunofluorescent, immunohistochemical and enzymehistochemical methods. The results indicated a decreased ratio of helper/inducer versus cytotoxic/suppressor T-lymphocytes, a remarkably high proportion of macrophages, a low frequency of IgE-producing plasma cells with different localization when compared with that of mast cells. These observations suggest that T-lymphocytes and macrophages may play an important role in the complex events of tissue destruction and repair taking place in the periapical region.
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PMID:Characterization of inflammatory cell infiltrate in dental periapical lesions. 833 Sep 36

The humoral immune response, especially IgG and IgA, is considered to be protective in the pathogenesis of periodontal disease, but the precise mechanisms are still unknown. Immunoglobulins arriving at the periodontal lesion are from both systemic and local tissue sources. In order to understand better the local immunoglobulin production, we examined biopsy tissue from periodontitis lesions for the expression of IgM, IgG, IgA, IgE and in addition the IgG and IgA subclasses and J-chain by in situ hybridization. Tissues examined were superficial inflamed gingiva and the deeper granulation tissue from periodontal sites. These data confirm that IgM, and IgG and IgA subclass proteins and J-chain can be locally produced in the periodontitis tissues. IgG1 mRNA-expressing cells were predominant in the granulation tissues and in the gingiva, constituting approx. 65% of the total IgG-expressing plasma cells. There was a significantly increased proportion of IgA-expressing plasma cells in the gingiva compared with the granulation tissue (P < 0.01). Most of the IgA-expressing plasma cells were IgA1, but a greater proportion expressed IgA2 mRNA and J-chain mRNA in the gingival tissues (30.5% and 7.5%, respectively) than in the periodontal granulation tissues (19% and 0-4%, respectively). The J-chain or dimeric IgA2-expressing plasma cells were located adjacent to the epithelial cells, suggesting that this tissue demonstrates features consistent with a mucosal immune response. Furthermore, we were able to detect the secretory component in gingival and junctional epithelial cells, demonstrating that the periodontal epithelium shares features with mucosal epithelium. In contrast, deeper tissues had more plasma cells that expressed IgM, and less expressing IgA, a response which appears more akin to the systemic immune response. In conclusion, this study suggests that immune mechanisms involved in the pathogenesis of periodontitis may involve features of both the mucosal and systemic immune systems, dependent on tissue location.
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PMID:Humoral immune responses in periodontal disease may have mucosal and systemic immune features. 1019 30

Patients infected with the human immunodeficiency virus (HIV) are highly susceptible to chronic marginal periodontitis (CMP) and the lesion is generally characterized by abundant plasma cell infiltration. HIV-induced reduction of CD4+ T cells may indirectly affect local production of immunoglobulins (Ig). Gingival biopsies taken from 10 HIV+ and 12 HIV- control patients with CMP were washed, fixed in ethanol and embedded in paraffin. Sections were examined after immunohistochemical staining with monoclonal antibodies against IgA, IgA1-2, IgG, IgG1-4, IgM and IgE. Ig-containing cells were counted in 3 separate connective tissue zones (subjacent to pocket epithelium, central zone and subjacent to oral epithelium). HIV+ patients showed a remarkably increased density of all Ig-containing cells in the connective tissue zone subjacent to the oral epithelium (p<0.05) and a lower % of IgG2+ cells in the entire gingival section (p<0.05). In HIV+ patients, the density of IgG-containing cells in the gingiva was strongly correlated with the serum IgG concentration. The altered topical distribution might imply impaired restriction of the inflammatory lesion, additional antigenic challenges by unusual microorganisms in the oral cavity, or be secondary to HIV-induced dysregulation of the B-cell system.
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PMID:The gingival plasma cell infiltrate in HIV-positive patients with periodontitis is disorganized. 1038 75


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