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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Periodontitis is a chronic inflammation of the supporting structures of the dentition which constitutes one of the most common causes of adult tooth loss. While certain microorganisms have been associated with the onset of the disease process, the exact pathogenetic mechanisms underlying periodontal destruction are still poorly understood. We have tested the hypothesis that gingival fibroblasts from diseased sites contribute to pathogenesis by possessing a secretory phenotype characterized by an exuberant secretion of inflammatory mediators and cytokines. Of the cytokines and mediators tested, fibroblast IL-1beta and prostaglandin E2 (PGE2) secretion was not different between health and disease. However, we have shown that fibroblasts from periodontal lesions produce in vitro greater amounts of IL-6 and IL-8 constitutively than healthy controls. When fibroblasts were stimulated with a panel of endogenous or exogenous response modifiers, the magnitude of cytokine and mediator stimulation above constitutive levels did not differ between health and disease. A strong positive correlation was identified between IL-6 or IL-8 constitutive secretion levels in vitro and the in situ expression of these cytokines within the connective tissues from where these cells originated, indicating that the in vitro phenotype mirrors their in vivo function. Furthermore, we present evidence which indicates that increased cytokine secretion by fibroblasts in disease is due to an elevated proportion of subpopulations with higher cytokine secretory capacity. Finally, we demonstrated that cultures from diseased sites are composed of cells with higher levels of constitutive CD40 expression, which may contribute to the increased IL-6 and IL-8 secretory phenotype.
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PMID:Increased presence of interleukin-6 (IL-6) and IL-8 secreting fibroblast subpopulations in adult periodontitis. 973 73

Freezing techniques provide a way of repeating and extending immunological assays by using frozen portions of an individual's peripheral blood mononuclear cell fraction. Earlier work shows that the lymphocytes that are stored frozen retain their ability to respond to polyclonal B-cell activators, mitogens, superantigens and bacterial extracts of oral interest. These studies extend previous findings by determining cytokine production by lymphocytes following frozen storage for up to 24 weeks. Production of interleukin (IL)-1beta, IL-2, IL-6, and tumour necrosis factor (TNF)-beta by stimulated lymphocytes after cyropreservation was not significantly different from those responses before storage, with one exception: IL-6 production was negligible after 24 weeks' frozen storage when thawed cells were cocultured with pokeweed mitogen. After stimulation with extracts from Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, the proliferative capacity of the frozen cells was maintained as well as the production of IL-1beta, IL-2, and IL-6. TNF-beta was not produced in response to bacterial antigen stimulation. The ability of peripheral blood mononuclear cells to retain functional activity after frozen storage should permit more effective monitoring during longitudinal clinical studies and a better evaluation of changes in cytokine production in patients with advanced periodontitis both during and after treatment.
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PMID:Cytokine production by cryopreserved human peripheral blood mononuclear cells in response to periodontal pathogens. 975 49

B-1 cells are physically and functionally unique B cells that produce polyreactive natural antibody. This study examined the activation of B-1 cells in inflamed gingival tissue. Serum IgG antibodies to phosphorylcholine, E. coli LPS, DNA, and some commensal bacteria were examined in adult periodontitis patients and healthy subjects. In addition, the proportion of B-1a (CD20+CD5+) cells and the amount of IL-6 and IL-10 in the inflamed gingival tissues were examined. The serum levels of IgG antibodies to phosphorylcholine, E. coli LPS, and commensal bacteria were significantly higher in the adult periodontitis patients than the healthy subjects. The proportion of B-1a cells and the amount of IL-6 and IL-10 were significantly higher in the inflamed gingival tissues than in peripheral blood from the healthy subjects. These results suggest the activation of B-1 cells in the inflamed gingival tissue of adult periodontitis patients, and that B-1 cells may serve as the first line of defense by producing polyreactive antibodies to phosphorylcholine, LPS, and commensal bacteria.
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PMID:Presence of activated B-1 cells in chronic inflamed gingival tissue. 985 87

Periodontitis is the inflammatory response in periodontal tissues elicited by bacterial colonization in periodontal pockets. In this response, pocket epithelial cells are the first cells to come into contact with bacteria. To elucidate this mechanism, we determined the adherence of the periodontopathic bacterium Eikenella corrodens 1073, which has a GalNAc-sensitive lectin-like adhesin (EcLS), to a human oral epithelial carcinoma cell line (KB) and the induction of proinflammatory cytokine production in the cells following exposure to this bacterium in vitro. In the adherence assay, EcLS played a role as the adhesin of this bacterium in adherence to KB cells. In a reverse transcriptase PCR, significant interleukin-8 (IL-8) and IL-6 mRNA levels were induced in response to exposure to this bacterium. In an enzyme-linked immunosorbent assay after an 8-h bacterial exposure, the IL-8 and IL-6 protein levels were 13.5- and 8.3-fold higher than those in the nonexposed controls, respectively. These protein responses were time dependent. Interestingly, when E. corrodens was separated from KB cells by cell culture inserts, a slight stimulation of the IL-6 and IL-8 mRNA and secreted protein levels was seen. These results imply that the direct contact of E. corrodens 1073 with oral epithelial cells is not necessarily required for the stimulation of IL-6 and IL-8 secretion. We suggest that E. corrodens induces the epithelial cells to secrete proinflammatory cytokines which serve as an early signaling system to host immune and inflammatory cells in underlying connective tissues.
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PMID:Interleukin-6 (IL-6) and IL-8 are induced in human oral epithelial cells in response to exposure to periodontopathic Eikenella corrodens. 986 40

Inflammatory mediators are central to the pathogenesis of periodontal diseases and may be used as markers in diagnosis. The aim of this study was to identify and quantify the various growth factors, apoptosis-related modifiers [soluble form of Fas (sFas) and bcl-2] and cytokines in the gingival crevicular fluid (GCF) of patients with different severities of periodontitis as compared with those of controls. GCF samples were taken from patients with periodontal disease and from controls. The concentrations of epidermal growth factor, transforming growth factor (TGF)-alpha, interleukin (IL)-1 beta, IL-6, interferon-gamma, beta 2-microglobulin (beta 2-MG), and apoptosis-related modifiers sFas and bcl-2 in the samples were determined by enzyme-linked immunosorbent assay. TGF-alpha was significantly lower in patients with periodontal disease than in the controls. In contrast, the concentrations of IL-1 beta, IL-6; and beta 2-MG were significantly higher in the group with severe periodontal disease than in the controls. The amount of total protein in the GCF was considerably higher in the disease group than the controls (p < 0.05). TGF-alpha, IL-1 beta, and beta 2-MG concentrations were associated (Spearman rank correlation, r < 0.05 for all) with clinical measures of disease severity (pocket depth) and inflammation (bleeding when probed). Apoptosis-related modifiers (sFas and bcl-2) could not be detected in any samples. These results suggest that the growth factor TGF-alpha and certain cytokines are associated with the presence of periodontal disease.
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PMID:Interleukin 1 beta, interleukin 6, beta 2-microglobulin, and transforming growth factor-alpha in gingival crevicular fluid from human periodontal disease. 1040 33

Deregulation of the cytokine network is an important adaptation of pathogenic bacteria to modulate and evade a host immune response. Here we describe that IL-6 is rapidly and efficiently cleaved and inactivated by the arginine- and lysine-specific proteinases from Porphyromonas gingivalis, referred to as RGP-A, RGP-B, and KGP. One of the primary cleavage sites for RGPs has been mapped between R18 and Q19 within the N-terminal region of the IL-6 polypeptide chain; however, both KGP and RGPs cleave IL-6 within the C-terminal region of the polypeptide chain. After these initial proteolytic cleavages, IL-6 is further degraded by each of the enzymes tested. Although KGP is the most potent IL-6-degrading proteinase, the initial C-terminal cleavage of IL-6 mediated by all gingipains is already sufficient to inactivate this cytokine. Our data are consistent with the observation that in periodontitis the IL-6 concentration is lowest in the gingival tissue adjacent to bacterial plaque, whereas significantly elevated concentrations of this cytokine are detected around the infected area. Degradation of IL-6 by gingipains may, therefore, represent an additional mechanism which influences the balance between pro- and anti-inflammatory reactions at distal versus proximal sites from the periodontal plaque.
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PMID:Rapid and efficient inactivation of IL-6 gingipains, lysine- and arginine-specific proteinases from Porphyromonas gingivalis. 1044 72

Campylobacter rectus is a periodontal pathogen with a 150-kDa protein on its cell surface. This protein forms a paracrystalline lattice, called the S-layer, surrounding the outer membrane of this gram-negative bacterium. To initiate a genetic analysis of the possible role of the S-layer in the initial interaction of C. rectus with host epithelial cells, C. rectus strains lacking the S-layer protein gene (crsA) were constructed by allelic exchange mutagenesis. Surprisingly, the lack of the S-layer had only a minor effect on the interaction of C. rectus with HEp-2 epithelial cells; CrsA(+) cells were 30 to 50% more adherent than were CrsA(-) bacteria. Since the host cell expression of cytokines appears to play an important role in the pathogenesis of periodontal diseases, the effect of the S-layer on the epithelial cell cytokine response was also examined by quantitative reverse transcriptase PCR and enzyme-linked immunosorbent assay. Although there were no changes in the mRNA levels for the anti-inflammatory cytokines interleukin-1 receptor agonist (IL-1ra), IL-13, and transforming growth factor beta, the expression and secretion of the proinflammatory cytokines IL-6, IL-8, and tumor necrosis factor alpha (TNF-alpha) were significantly induced by both wild-type C. rectus and CrsA(-) bacteria. Interestingly, the kinetics of cytokine induction differed for the CrsA(+) and CrsA(-) bacteria. At early time points, the HEp-2 cells challenged with CrsA(-) bacteria produced higher levels of IL-6, IL-8, and TNF-alpha mRNA and protein than did cells challenged with CrsA(+) bacteria. We conclude that C. rectus may help initiate periodontitis by increasing the expression of proinflammatory cytokines and that the S-layer may temper this response to facilitate the survival of C. rectus at the site of infection.
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PMID:Use of defined mutants to assess the role of the Campylobacter rectus S-layer in bacterium-epithelial cell interactions. 1067 61

Periodontitis is characterized by an inflammatory process induced by periodontopathogenic bacteria in the subgingival plaque. Periodontal inflammation can be enhanced by both an increase of inflammatory stimulators, e.g. interleukin (IL)-6, and a decrease of inflammatory inhibitors, e.g. IL-10. The amount of IL-1beta is known to be increased in gingival tissues and in the gingival crevicular fluid from inflamed sites compared to healthy sites. This in vitro study sought to clarity whether IL-1beta (1 ng/ml) has a regulatory effect on the release of these two cytokines from human periodontal ligament (PDL) cells. PDL cells derived from healthy premolars were grown in the presence and absence (control) of IL-1beta. The concentration of IL-6 and IL-10 in the supernatants was assessed by enzyme-linked immunosorbent assay after 48 h of culture. PDL cells incubated with IL-1beta released significantly (p < 0.05) higher amounts of IL-6 and significantly (p < 0.01) smaller amounts of IL-10 compared to control. These results give further support to the observation that IL-1beta can increase the IL-6 secretion from PDL cells. Moreover, they provide original evidence that PDL cells secrete IL-10, which can be suppressed by IL-1beta. It is concluded that PDL cells can function as accessory immunoinflammatory cells amplifying the inflammatory process in periodontitis and, thereby, contributing to periodontal breakdown.
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PMID:Suppression of interleukin-10 release from human periodontal ligament cells by interleukin-1beta in vitro. 1071 23

We examined the induction of the cytokines interleukin (IL)-1 beta, IL-6, and IL-8 by lipopolysaccharides (LPSs) from several species of possible endodontopathic black-pigmented bacteria. Studies were conducted in human whole blood cultures from six patients (two from each group) with differing numbers of periapical periodontitis lesions (i.e. patients with radiographically clear periapical lesions in 10 or more teeth (high-lesion group, n = 4), in one or two teeth (low-lesion group, n = 6), and six healthy volunteers with no periapical lesions (no lesion group)). LPS from Prevotella intermedia ATCC 25611, Porphyromonas gingivalis 381, and Prophyromonas endodontalis ATCC 27067 induced a higher IL-8 response in the subjects of the high-lesion group, compared with the subjects of the other two groups. To ascertain the degree of sensitization by test bacteria, we examined the reactivities of antibodies in serum and saliva from the subjects to different bacterial species. LPS from P. gingivalis reacted strongly with sera from the high-lesion group. Thus, LPS from black-pigmented bacteria may be involved in multilesional periapical periodontitis by inducing particular cytokines and/or humoral immune responses.
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PMID:Inflammatory cytokine production and specific antibody responses to lipopolysaccharide from endodontopathic black-pigmented bacteria in patients with multilesional periapical periodontitis. 1072 23

Diabetes is associated with increased prevalence, severity, and progression of periodontal disease. To test the hypothesis that activation of RAGE (Receptor for Advanced Glycation End products) contributes to the pathogenesis of diabetes-associated periodontitis, we treated diabetic mice, infected with the human periodontal pathogen Porphyromonas gingivalis, with soluble RAGE (sRAGE). sRAGE is the extracellular domain of the receptor, which binds ligand and blocks interaction with, and activation of, cell-surface RAGE. Blockade of RAGE diminished alveolar bone loss in a dose-dependent manner. Moreover, we noted decreased generation of the proinflammatory cytokines TNF-alpha and IL-6 in gingival tissue, as well as decreased levels of matrix metalloproteinases. Gingival AGEs were also reduced in mice treated with sRAGE, paralleling the observed suppression in alveolar bone loss. These findings link RAGE and exaggerated inflammatory responses to the pathogenesis of destructive periodontal disease in diabetes.
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PMID:Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice. 1077 56


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