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)

Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that peripheral blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL-1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T-cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria-specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies, Actinobacillus actinomycetemcomitans (Aa)-specific T-cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM-1, LECAM-1 and PECAM-1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T-cell clones homing to the gingiva in CIPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunopathogenesis of chronic inflammatory periodontal disease: cellular and molecular mechanisms. 750 22

Differences in lymphocyte populations have been demonstrated in gingivitis and periodontitis lesions. A differential expression of adhesion molecules may play a role in lymphocyte trafficking in these tissues. An indirect avidin biotin immunoperoxidase technique was used to stain a range of adhesion molecules in tissue sections of 21 gingival biopsies from both gingivitis and periodontitis subjects. These specimens were placed into three groups according to the size of the infiltrate. ICAM-1, PECAM-1 and LECAM-1 expression on mononuclear cells in the inflammatory infiltrates increased significantly with increasing size of infiltrate. Approximately 50% of these mononuclear cells were LFA-1+ and CD29+. When specimens were grouped according to their putative disease status there were no significant differences between mononuclear cell adhesion molecule expression in small infiltrates from either gingivitis or adult periodontitis subjects. This was also the case with larger lesions from both clinical groups. Therefore there does not appear to be a differential expression of adhesion molecules on lymphocytes in gingivitis and periodontitis tissue. Endothelial cells were positive for ICAM-1, PECAM-1, CD29, GMP-140 but negative for ELAM-1. Keratinocyte expression of ICAM-1 increased with increasing size of infiltrate although in heavy infiltrates, cells in the region of the junctional epithelium which were positive in small lesions, became ICAM-1 negative. The upper layers of the oral epithelium were positive for LECAM-1 in small infiltrates and with increasing size of infiltrate, the lower layers and many of the sulcular and junctional epithelium keratinocytes were positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adhesion molecule expression in chronic inflammatory periodontal disease tissue. 750 85

T cell induced differentiation of B cells has been shown to be dependent on the CD2/LFA-3 and LFA-1/ICAM-1 pathways. Flow cytometric analysis was used to examine these adhesion molecules on T and B cells extracted from gingival tissues before and after stimulation with the putative periodontopathic bacteria, Porphyromonas gingivalis and Fusobacterium nucleatum. Adhesion molecule expression on peripheral blood cells from healthy adults was used as a control. Approximately 50 per cent of B cells extracted from gingival tissues expressed LFA-3 and ICAM-1 compared with 30 per cent positive peripheral blood B cells. Around 50 per cent of gingival T cells expressed CD2 relative to 76 per cent positive peripheral blood T cells. However, 40-50 per cent of both gingival and peripheral blood T cells expressed LFA-1. There was no difference in the expression of adhesion molecules on T and B cells extracted from health/marginal gingivitis or adult periodontitis lesions. After stimulation of gingival cells in vitro, the per cent CD2 positive T cells and LFA-3 and ICAM-1 positive B cells remained relatively stable over the six-day culture period, although P. gingivalis and F. nucleatum appeared to induce an increase in the percentage of gingival T cells expressing LFA-1. In contrast to the gingival lymphocytes, stimulation of peripheral blood cells resulted in an increase in the per cent CD2 positive T cells, LFA-3 and ICAM-1 positive B cells, with a decrease in LFA-1 positive T cells. The results therefore demonstrated that gingival T and B cells express adhesion molecules in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular adhesion molecules on periodontal lymphocytes. 754 Mar 89

Activated T lymphocytes constitute a major component of inflammatory cells in the early periodontal lesion, and also appear in the gingival crevicular fluid. In an attempt to clarify the relationship between the ICAM-1 (CD54) expression of pocket epithelium in gingiva and the infiltrating lymphocyte population, we carried out an analysis of CD11a+(LFA-1 alpha), CD25+(IL-2R alpha) and CD4+(Th) cells subjacent to ICAM-1-expressing pocket epithelia and CD11a+CD25+CD4+ cells in gingival crevicular fluid (GCF). GCF was collected by crevicular washing from 16 patients with periodontitis (P group) and 3 subjects with healthy gingiva (H group). Peripheral blood (PB) was collected at the same time. Mononuclear cells were isolated by Ficoll-paque gradient centrifugation from GCF and PB. Monoclonal antibodies (mAb) to CD11a, CD25, and CD4 were used for three-color flow cytometry. Gingival biopsies were obtained from 7 patients in P group and 3 subjects in H group. Serial cryostat sections (6 microns in thickness) were prepared from each biopsy, on which a double staining was performed. The number of CD11a+CD25+CD4+ cells and the fluorescence intensity of FITC conjugated anti-CD11a were significantly higher in GCF than in PB (p < 0.001 to p < 0.01). CD11a+CD25+CD4+ cells were not detected in GCF in H group. The pocket epithelia expressed CD54 in P group, but not in H group. The number of CD11a+, CD25+ and CD4+ cells infiltrating the connective tissue subjacent to the upper, middle and lower parts of the CD54 positive pocket epithelium (n = 16) was 141 +/- 26, 38 +/- 13, 144 +/- 29 (cells/0.04 mm2), respectively, whereas in the CD54 negative pocket epithelium, it was (n = 5) 9 +/- 2, 3 +/- 1, 8 +/- 3. In P group, the CD11a+CD25+CD4+ cell number in GCF correlated with CD25+, CD11a+ cells in the connective tissue subjacent to the CD54+ pocket epithelium. These results indicate that expression of ICAM-1 in pocket epithelium is relevant to the migration of CD11a, CD25, CD4 positive cells in connective tissue subjacent to the pocket epithelium into the periodontal pocket. Assessing the relationship of our findings and other adhesion molecules would offer important clues to the understanding of T cell migration in affected gingiva.
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PMID:ICAM-1-expressing pocket epithelium, LFA-1-expressing T cells in gingival tissue and gingival crevicular fluid as features characterizing inflammatory cell invasion and exudation in adult periodontitis. 854 7

Chronic adult periodontitis is usually characterized by inflammatory cell accumulation in the extravascular periodontal connective tissue. In order to reveal how the lymphocyte migration and retention in periodontal lesions is regulated, we have focused on the molecular basis for the adhesive interactions between lymphocytes and human gingival fibroblasts (HGF). In this study, we investigated the involvement of cell adhesion molecules in adhesive interactions between lymphocytes and HGF. We found that activated lymphocytes bound strongly to HGF and VLA integrins, extracellular matrix receptors, play crucial roles in the binding. Interestingly, we first revealed that CD44 molecules (hyaluronate receptor) on lymphocytes also participated in lymphocyte-HGF interactions and that hyaluronate anchored on the surface of HGF functioned as the ligand for CD44. In addition, when HGF were stimulated with inflammatory cytokines such as IL-1, TNF alpha and IFN gamma, the binding avidity between lymphocytes and HGF was significantly increased and the adhesion was mainly mediated by LFA-1/ICAM-1 pathway. We then examined the possibility whether lymphocyte-HGF interaction may cause activation of HGF. When HGF directly interacted with lymphocytes for 3 h, IL-1 beta mRNA expression was clearly increased in HGF. These findings suggested that the adhesive interactions between lymphocytes and HGF was mediated at least by VLA integrins, LFA-1/ICAM-1 and CD44/hyaluronate and that the heterotypic cell-cell interactions could mutually cause intracellular signal transduction.
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PMID:Immunoregulatory roles of adhesive interactions between lymphocytes and gingival fibroblasts. 908 19

Porphyromonas gingivalis is thought to be one of the major pathogenic organisms of adult periodontitis. Of the several virulence factors associated with the pathology it causes, evidence is now presented suggesting that outer membrane vesicles, which form from blebbing of the outer membrane, may also contribute to the pathogenesis of this bacterium. To evaluate this possibility, outer membrane vesicles were isolated from cultures of P. gingivalis and tested for their ability to promote inflammation and for their effects on the biosynthesis of E-selectin and ICAM-1 adhesion molecules and MHC class II glycoproteins. The results indicate that these vesicles are capable of inducing acute inflammation characterized by the accumulation of a large number of neutrophils in the connective tissue. This cellular response corresponds to the vesicle-mediated biosynthesis and surface membrane expression of E-selectin and ICAM-1 by vascular endothelial cells. In contrast, IFN-gamma-dependent synthesis of MHC class II molecules was found to be inhibited by vesicles. Inhibition of HLA-DR expression occurred regardless of whether vesicles were added at the same time as, 24 h before, or 24 h after IFN-gamma stimulation of endothelial cells, suggesting that the inhibitory effects occur at both the membrane and intracellular level. These findings, taken together, indicate that P. gingivalis membrane vesicles are capable of inducing and regulating cellular responses involved in inflammation and initiation of acquired immunity. Membrane vesicles are composed of muramyl peptides, periplasmic proteins and outer membrane constituents. The combination of these components probably contribute to the immune regulatory functions reported herein.
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PMID:Outer membrane vesicles of Porphyromonas gingivalis inhibit IFN-gamma-mediated MHC class II expression by human vascular endothelial cells. 1045 19

Because of their importance in mediating cellular interactions in chronic inflammatory diseases, this study has examined the expression of a number of adhesion molecules in adult (n=11), generalized early onset (n=5) and localized early onset (n=2) forms of periodontitis. In comparison with immunostaining profiles of cryostat sections of healthy gingival tissue (n=7), the beta 1 integrins VLA-1, VLA-2 and VLA-4 were found to be up-regulated in periodontitis, with VLA-6 being markedly elevated. Although only small differences were observed in ICAM-1 and LFA-3 expression in the gingival epithelium, there was particularly notable up-regulation of these adhesion molecules within the inflammatory infiltrates of the diseased tissues. However, there were no statistically significant differences between the serum levels of a soluble form of LFA-3 in periodontitis patients (n=47) compared with healthy control subjects (n=40), although the generalized early onset and adult periodontitis groups exhibited wider ranges of circulating LFA-3. These findings show that there is localized modulation of adhesion molecule expression in the chronic inflammatory periodontal diseases studied, but that the levels of LFA-3 in the circulation nevertheless remain unaffected.
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PMID:Localized adhesion molecule expression and circulating LFA-3 levels in adult and early onset forms of periodontitis. 1059 6

Migration of leukocytes to inflammation sites through vascular endothelium is controlled by the interactions of adhesion molecules expressed on both endothelial cells and leukocytes, most of which are already covered by cluster of differentiation (CD) codes. We examined the expression of a variety of endothelial cell adhesion molecules in human dental pulp vasculature to obtain further evidence on the tissue distribution and function of these molecules by using an indirect immunoperoxidase technique. We obtained the pulp tissue samples from teeth extracted due to orthodontic reasons as controls and compared with those extracted due to chronic periodontitis. In all samples, both CD31 and CD146 were expressed by arterial, venous, and capillary endothelia. There was no significant difference between the staining intensity of normal and inflamed pulp tissues. CD102 expression on the endothelium was significantly stronger in chronic periodontitis pulp samples. CD106, CD62-E, CD62-P, CD105, and CD54 were variably expressed in control and chronic periodontitis groups. Our results indicate that CD102 represents the major endothelial cell adhesion molecule probably involved in the inflammatory reactions in chronic periodontitis.
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PMID:Endothelial cell adhesion molecules in human dental pulp: a comparative immunohistochemical study on chronic periodontitis. 1068 24

Cysteine proteinases (gingipains) elaborated from Porphyromonas gingivalis exhibit enzymatic activities against a broad range of host proteins and are considered key virulence factors in the onset and development of adult periodontitis and host defense evasion. In this study, we examined the ability of arginine-specific gingipains (high molecular mass Arg-specific gingipain (HRGP) and Arg-specific gingipain 2) and lysine-specific gingipain (KGP) to cleave monocyte CD14, the main receptor for bacterial cell surface components such as LPS. Binding of anti-CD14 mAb MY4 to human monocytes was almost completely abolished by 0.3 microM HRGP and KGP treatments for 15 min, and 1 microM RGP2 for 30 min. In contrast, the expressions of Toll-like receptor 4, and CD18, CD54, CD59, and HLA-A, -B, -C on monocytes were slightly increased and decreased, respectively, by 0. 3 microM HRGP and KGP. This down-regulation resulted from direct proteolysis, because 1) gingipains eliminated MY4 binding even to fixed monocytes, and 2) CD14 fragments were detected in the extracellular medium by immunoblot analysis. Human rCD14 was degraded by all three gingipains, which confirmed that CD14 was a substrate for gingipains. TNF-alpha production by monocytes after HRGP and KGP treatments was decreased at 1 ng/ml, but not at 20 microg/ml LPS, indicating that gingipains inhibited a CD14-dependent cell activation. These results suggest that gingipains preferentially cleave monocyte CD14, resulting in attenuation of the cellular recognition of bacteria, and as a consequence sustain chronic inflammation.
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PMID:Proteolysis of human monocyte CD14 by cysteine proteinases (gingipains) from Porphyromonas gingivalis leading to lipopolysaccharide hyporesponsiveness. 1086 Oct 79

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


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