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 frequency of disease for children who were breast fed as babies is lower than that for children who were bottle fed. Breast milk contains specific and nonspecific proteins which act against pathogens. The influence of breast milk on the development of juvenile periodontitis was examined. It was shown that, out of 55 children raised on bottle milk, 9 children up to 14 years of age showed inflammatory changes in the gingiva while only 1 child out of the 17 fed with breast milk during the first few months of life had gingivitis. The lower frequency of gingivitis can probably be explained by the immunopathology of periodontitis.
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PMID:[Dental studies on the protective effect of breast feeding]. 28 63

Eubacterium brachy, a gram-positive anaerobic rod, has been implicated by cultural studies to be associated with the microflora of periodontal diseases. Serum samples from 184 clinically characterized patients were evaluated in a standardized enzyme-linked immunosorbent assay (ELISA) for reactivity to E. brachy antigens. Sera from clinically healthy subjects (HS) served as controls. Sera from rapidly progressive periodontitis (RP) patients demonstrated significantly greater reactivity by ELISA than did HS when reactivity with E. brachy antigens was determined (P less than 0.05). Juvenile periodontitis (JP) and adult periodontitis (AP) patients did not differ in reactivity by ELISA from HS (P greater than 0.05). Three to 4 years following successful periodontal therapy, reactivity was not significantly altered in any patient group (P greater than 0.05). The possible significance of these findings and the importance of an extracellular antigen of E. brachy in the immunopathology of periodontal diseases are discussed.
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PMID:Systemic antibody response of clinically characterized patients with antigens of Eubacterium brachy initially and following periodontal therapy. 346 34

Gingival biopsy specimens from 20 patients with moderate to advanced periodontitis were obtained from inflamed sites with pockets of 5 mm or more. Sections were studied by an immunofluorescence technique, using polyclonal rabbit or goat anti-IgG, anti-IgM, anti-C1q, anti-C3a, and anti-C3c and mouse monoclonal anti-C9. Prewashed ethanol-fixed and nonwashed ethanol-fixed or frozen specimens showed many plasma cells staining for IgG or C3a, suggesting the possible occurrence of a receptor for C3a in plasma cells. Plasma cells containing IgM were also seen. Deposits of IgG and IgM with C1q, C3a, and C3c, suggesting immune complexes, were demonstrated by a double staining technique, combining fluorescein (FITC) or rhodamine (TRITC)-labeled anti-immunoglobulins with TRITC- or FITC-conjugated antibody to C3a, C3c, and C1q. The complexes were located mainly within or around vessel walls. Deposits of C3a and C1q were found in vessel walls, in the basement membrane zone of oral gingival epithelium, or diffusely distributed in the tissues. Deposits of C3c were found to a lesser extent and only in vessel walls. Mouse monoclonal anti-C9, visualized with FITC-labeled rabbit anti-mouse and swine anti-rabbit antiserum, showed granular deposits of C9, mainly in the basement membrane zone of oral gingival epithelium. The study indicates the involvement of immune complex vasculitis in inflammatory periodontal lesions. Also, our observations of the occurrence of deposits of complement factors support the hypothesis that complement factors play an important role in the immunopathology of the periodontal lesion.
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PMID:Deposits of immunoglobulins, complement, and immune complexes in inflamed human gingiva. 349 17

Recent studies have demonstrated an association of Eubacterium sp. with the subgingival microflora of patients with chronic periodontitis. One species, Eubacterium brachy, was evaluated to determine the possible mechanisms by which this microorganism may contribute to these diseases. Of 167 sera evaluated by double diffusion in agar, 20.8% displayed reactivity with a sonicated preparation of E. brachy. An extracellular antigen was identified in the culture supernatant fluid which reacted with antibodies in human sera. This antigen was isolated by methanol precipitation and purified by gel filtration. When tested by an enzyme-linked immunosorbent assay, all sera displayed some reactivity. Lines of identity were not shared with other species of Eubacterium, but were shared with other clinical isolates of E. brachy. The reactive antibody was identified as immunoglobulin G by immunoelectrophoresis, verified by enzyme-linked immunosorbent assay, and found to be capable of complement fixation. The monosaccharides and amino acids of the extracellular antigen were identified by high-pressure liquid chromatography. This antigen was shown to have a molecular weight of 170,000 and to share a line of identity with the sonicated preparation of E. brachy. The possible role of the organism in the immunopathology of periodontal diseases is discussed.
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PMID:Reaction of human sera with Eubacterium brachy: isolation and characterization of an extracellular antigen. 397 41

The immunopathology of T4 & T8 cell subsets in gingival tissues from 20 patients affected with either juvenile (JP) or rapidly progressive periodontitis (RPP) were studied using immunoperoxidase method for monoclonal antibodies of T4 & T8. Results were compared with gingival samples taken from systemically and periodontally healthy subjects. T4 subsets were found to be significantly elevated in JP & RPP, when compared with controls. Yet it was found to be higher in JP than in RPP, while T8 subsets were found to be depressed in both types of diseases. Those findings could contribute to the immunopathogenesis of JP & RPP.
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PMID:Immunopathology of T-lymphocyte subsets in juvenile and rapidly progressive periodontitis. 958 40

In this study, we investigated the relative proportions of infiltrating mononuclear inflammatory cells in sections of granulation tissue from periodontitis lesions in both adult periodontitis (AP) and early onset periodontitis (EOP) patients. We utilised a set of cluster of differentiation (CD) antigen-specific monoclonal antibodies to detect different cell types within the tissues. These included anti-CD 20 (B cells), anti-CD 3 (pan T cells) and anti-CD 45RO (memory T cells), anti-CD 4 (helper T cells) anti-CD 8 (suppressor T cells) and anti-CD 68 (monocyte/macrophage). Biopsies of granulation tissue were obtained from 9 patients with adult periodontitis (AP), from 10 patients with early onset periodontitis (EOP) and for comparative purposes, biopsies of gingival tissue from 4 patients with AP. A significantly greater number of T cells (p < 0.05) were observed in EOP and gingival sections than in AP sections. In addition, a greater number of B cells were observed in the granulation tissues than in the gingiva (p < 0.05). The relative numbers of B cells (CD 20). T cells (CD 3) and macrophages (CD 68) were expressed as a percentage of their combined total for each of the patient groups and indicated that the proportion of B lymphocytes was greater in AP sections than in EOP or gingival sections (p < 0.02). The proportion of T cells was lower in the AP periodontitis sections than in the EOP periodontitis sections (p < 0.05). There were no significant differences in the proportion of macrophages between the 3 categories of tissue specimens. The relative ratios of B cells (CD 20) to T cells (CD 3) and B cells (CD 20) to memory T cells (CD 45RO) and macrophages (CD 68) to T cells (CD 3) and memory T cells (CD 45RO) were analyzed and indicated that there was a significant increase in the B to T cell ratio in AP sections compared to EOP and gingival sections (p < 0.02). There was also a significant increase in the macrophage to T cell ratio in AP sections as indicated by CD 68 to CD 3 ratios (p < 0.05). There were no differences regarding the relative proportions of memory T cells or in the ratios of CD 4+ to CD 8+ T cells in the different disease categories. In conclusion, these differences in the relative proportions of B cells, T cells and macrophages may reflect a difference in the immunopathology of AP and EOP.
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PMID:Relative proportions of mononuclear cell types in periodontal lesions analyzed by immunohistochemistry. 1010 45

Interleukin 12 (IL-12) is an efficient inducer and enhancer of gamma interferon (IFN-gamma) production by both resting and activated T cells. There is evidence that human monocytes exposed to IFN-gamma have enhanced ability to produce IL-12 when stimulated with lipopolysaccharide (LPS). In this study, it was demonstrated that LPS from the oral periodontal pathogen Porphyromonas gingivalis stimulated monocytes primed with IFN-gamma to release IL-12, thereby enhancing IFN-gamma accumulation in T-cell populations. P. gingivalis LPS was shown to enhance IL-12 induction of IFN-gamma in T cells in a manner independent from TNF-alpha contribution. The levels of T-cell IL-12 receptors were not affected by P. gingivalis LPS and played only a minor role in the magnitude of the IFN-gamma response. These data suggest that LPS from P. gingivalis establishes an activation loop with IL-12 and IFN-gamma with potential to augment the production of inflammatory cytokines in relation to the immunopathology of periodontitis. We previously reported that the major cysteine proteinases (gingipains) copurifying with LPS in this organism were responsible for reduced IFN-gamma accumulation in the presence of IL-12. However, the addition of the gingipains in the presence of LPS resulted in partial restoration of the IFN-gamma levels. In the destructive periodontitis lesion, release of gingipains from the outer membrane (OM) of P. gingivalis could lead to the downregulation of Th1 responses, while gingipain associated with LPS in the OM or in OM vesicles released from the organism could have net stimulatory effects.
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PMID:Modulation of an interleukin-12 and gamma interferon synergistic feedback regulatory cycle of T-cell and monocyte cocultures by Porphyromonas gingivalis lipopolysaccharide in the absence or presence of cysteine proteinases. 1222 99

Human immunoglobulin G2 (IgG2) responses are gamma interferon (IFN-gamma) dependent, and monocyte-derived dendritic cells (mDCs) promote IgG2 production. DCs spontaneously emerge from monocytes in cultures prepared from localized aggressive periodontitis (LagP) patients, and these patients have high levels of IgG2 that is reactive with Actinobacillus actinomycetemcomitans. These results prompted the hypothesis that an interaction between mDCs and A. actinomycetemcomitans promotes IFN-gamma production, and IFN-gamma is known to promote both immunopathology and protective IgG2. A. actinomycetemcomitans induced mDCs to produce interleukin-12 (IL-12), and the addition of A. actinomycetemcomitans and DCs to cultured peripheral blood lymphocytes elicited high levels of IFN-gamma within just 24 h. In contrast, IL-4 was not detectable although DC-derived IL-10 production was apparent. A. actinomycetemcomitans-stimulated macrophages prepared from the same monocytes lacked the ability to induce IL-12 or IFN-gamma responses. NK cells of the innate immune system were the primary source of this early IFN-gamma, although CD8 T cells also contributed some. The NK cell-derived IFN-gamma was IL-12 dependent, and A. actinomycetemcomitans-DC interactions were Toll-like receptor 4 dependent. A. actinomycetemcomitans and A. actinomycetemcomitans lipopolysaccharide (LPS) were more potent than Escherichia coli and E. coli LPS in the ability to induce DC IL-12 and IFN-gamma. The ability of A. actinomycetemcomitans-stimulated DCs to induce NK cells to rapidly produce IFN-gamma in the absence of detectable IL-4 suggests their potential for skewing responses toward Th1. This may help explain the presence of Th1-associated cytokines in gingival crevicular fluid (GCF) from LagP patients and the high levels of IgG2 in their serum and GCF that is reactive with A. actinomycetemcomitans.
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PMID:Dendritic cells stimulated with Actinobacillus actinomycetemcomitans elicit rapid gamma interferon responses by natural killer cells. 1532 2

In this study, infiltrating lymphocytes subpopulation in gingival sections of healthy, inflamed, and periodontitis lesions was investigated. A set of cluster of differentiation (CD) antigen specific monoclonal/polyclonal antibodies to detect different cell types within the tissues was used. These included anti-CD3 (pan T-cell), anti-CD45RO (memory T-cell), anti-CD20 (B-cell), and kappa light chain (plasma cells). Biopsies of gingival tissue were obtained from 17 patients who had clinically healthy gingiva, from 18 patients with gingivitis, and 17 patients with periodontitis.A significantly greater proportion of T-cells (P < 0.00) was observed in healthy gingival and gingivitis tissue samples compared to periodontitis tissue samples. In addition, a greater proportion of B-cells was observed in periodontitis lesions than in the gingival lesions (P < 0.00). The memory T-cells and the kappa light-chain plasma cells were present in both healthy and diseased tissues, suggestive of previous activation by periodontal pathogenic microorganisms.In conclusion, these differences in the relative proportions of B- and T-cells may reflect a difference in the immunopathology of periodontitis and gingivitis lesions.
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PMID:Lymphocyte subpopulation in healthy and diseased gingival tissue. 2014 44

Although the complement system is centrally involved in host defense, its overactivation or deregulation (e.g., due to inherent host genetic defects or due to pathogen subversion) may excessively amplify inflammation and contribute to immunopathology. Periodontitis is an oral infection-driven chronic inflammatory disease which exerts a systemic impact on health. This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencies in specific complement components appear to predispose to increased susceptibility to periodontitis. Animal model studies and in vitro experiments indicate that periodontal bacteria can either inhibit or activate distinct components of the complement cascade. Porphyromonas gingivalis, a keystone species in periodontitis, subverts complement receptor 3 and C5a anaphylatoxin receptor signaling in ways that promote its adaptive fitness in the presence of non-productive inflammation. Overall, available evidence suggests that complement activation or subversion contributes to periodontal pathogenesis, although not all complement pathways or functions are necessarily destructive. Effective complement-targeted therapeutic intervention in periodontitis would require determining the precise roles of the various inductive or effector complement pathways. This information is essential as it may reveal which specific pathways need to be blocked to counteract microbial evasion and inflammatory pathology or, conversely, kept intact to promote host immunity.
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PMID:Complement and periodontitis. 2059 85


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