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)

This study aimed to investigate whether circulating neutrophils from patients with periodontitis contain more catalytically active elastase than neutrophils from healthy controls. The amount of IL-1beta in these cells was also analyzed and the correlation with elastase activity was tested. The periodontitis group consisted of 15 subjects with marked periodontal destruction. The healthy control group consisted of 15 subjects with no clinical signs of periodontal destruction. The elastase activity and the IL-1beta content in the cells were measured with flow cytometry using a specific substrate and antibodies, respectively. The plasma concentration of IL-1beta and the total content of antigenic elastase in the crushed cells were measured with an ELISA. The elastase activity per neutrophil was significantly higher in the patients than in the controls, while the total antigenic elastase content did not differ. The % of cells positively stained for IL- 1beta was somewhat higher in the patient group. Significantly higher amounts of IL-1beta per sample, estimated by multiplying the % of stained cell with the amount of staining per cell, were found in the patient group. A significant correlation between IL-Ibeta and elastase activity was noted in the patient group (R=0.6, p=0.001), but not in the control group. In conclusion, peripheral neutrophils from patients with adult periodontitis express more active elastase and total amounts of IL-1. The similar amounts of antigenic elastase suggests that this higher activity is possibly due to some kind of priming/activation already in the circulation.
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PMID:Expression of intracellular elastase activity in peripheral neutrophils from patients with adult periodontitis. 1095 83

Bacteriological and cytological analysis of the saliva, dental plaques, and gingival fluid was carried out in 48 patients with periodontitis and 25 donors. The concentrations of proinflammatory cytokines IL-1 and TNF-alpha were increased, the levels of anti-inflammatory cytokines IL-4 and TFR beta-1 were decreased, and MIF production was suppressed in the patients in comparison with donors. Important theoretical and practical recommendations are offered.
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PMID:[A comprehensive study of the mechanisms of the development of chronic inflammation in periodontitis]. 1096 Nov 5

The effect of two arginine-specific cysteine proteinases (gingipains R) from Porphyromonas gingivalis, an aetiological factor of adult periodontitis, on the activation of human factor IX was investigated in the presence of ethylene glycol, an activity enhancer of activated factor IX (factor IXa), with the use of a fluorogenic oligopeptide substrate. Each gingipain R rapidly activated factor IX but the 95 kDa proteinase complex (HRgpA) that contains both haemagglutinin/adhesion and catalytic domains was 2.4-fold more efficient than the single-chain 50 kDa gingipain R (RgpB), which has only a catalytic domain. SDS/PAGE and N-terminal sequence analysis of factor IX digestion fragments indicated that, like all endogenous activators, gingipains R also produce factor IXabeta via an IXa intermediate. Significantly, phospholipids augmented the activation of factor IX by HRgpA but not by RgpB in a Ca(2+)-dependent manner. In the presence of both cofactors the kinetic efficiency of HRgpA to activate factor IX (k(cat)/K(m)=1.9x10(6) M(-1).s(-1)) was 8.5-fold higher than that of RgpB (k(cat)/K(m)=2.3x10(5) M(-1).s(-1)) and double that of the factor VIIa-tissue factor complex, but 8-fold lower than that for factor XIa. A comparison of the relative activation rates of factor IX, factor X and prothrombin directly in plasma by HRgpA suggests a significant contribution for factor IX conversion in blood coagulation induced by gingipains R. Taken together, gingipains R are the first-reported activators of factor IX of bacterial origin. By this effect they could be involved in the production of thrombin as well as the subsequent generation of prostaglandins and interleukin 1, all of which have been found to be associated with the development and progression of periodontitis.
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PMID:Activation of blood coagulation factor IX by gingipains R, arginine-specific cysteine proteinases from Porphyromonas gingivalis. 1113 97

Specific bacteria cause periodontitis by activating immuno-inflammatory responses in the tissues. There are certain risk factors that significantly affect the disease process by altering the immuno-inflammatory response and increasing the likelihood of severe periodontitis. These risk factors are smoking, diabetes, IL-1 genotype, and perhaps others. Today about 20 percent of the population smokes at a level that should make a difference relative to periodontitis. About 30 to 33 percent of the Caucasian population is IL-1 genotype positive. There are compelling reasons to look at these risk factors in your practice to help formulate a complete treatment plan for your patients.
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PMID:Is periodontitis genetic? The answer may be Yes! 1132 54

This review examines a well-characterized factor, interleukin 1 (IL-1), that has recently received considerable attention. A level of understanding is emerging that goes beyond simple recognition that IL-1 plays a role in disease, and begins to explain the molecular mechanisms of function. This review summarizes some current information on the importance of IL-1 in periodontitis as well as the signal transduction of IL-1, from binding to its cell-surface receptors, to the activation of cytoplasmic mediators and transcription factors responsible for the induction of target genes. The effect of IL-1 signal transduction is ultimately the activation and repression of specific transcription factors that regulate genes responsible for cellular activities. As additional steps of signal transduction become better-characterized, these insights may facilitate the development of improved therapeutic approaches for controlling inflammation and connective tissue destruction in a variety of diseases.
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PMID:Interleukin 1 signal transduction--current concepts and relevance to periodontitis. 1133 22

IL-1 is secreted by a variety of cells and plays an important role in the network of cytokines. In this study, the expression of IL-1 alpha in gingival tissue was determined with reverse transcription-polymerase chain reaction (RT-PCR). The PCR-product was confirmed by DNA sequencing. The results showed that IL-1 alpha transcription was detected in all 5 inflammatory gingival tissue samples, but it was not delected in the normal gingival tissue samples and in the samples after treatment. These findings suggested that IL-1 alpha may be a specific indicator of periodontal disease, and a potential mediator in pathogenesis of periodontitis.
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PMID:[The expression of IL-1 alpha gene in gingival tissue]. 1148 49

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.
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PMID:[Induction of histidine decarboxylase in inflammation and immune responses]. 1149 27

Numerous studies have attempted to elucidate the cytokine networks involved in chronic periodontitis, often with conflicting results. A variety of techniques were used to study cells in situ, cells extracted from gingival tissues, peripheral blood mononuclear cells, purified cell populations, and T cell lines and clones. Bacterial components, including sonicates, killed cells, outer membrane components, and purified antigens, have all been used to stimulate cells in vitro, making comparisons of cytokine profiles difficult. As it is likely that different cells are present at different disease stages, the inability to determine disease activity clinically is a major limitation of all these studies. In the Context of tissue destruction, cytokines such as IL-1, IL-6 and IL-18 are likely to be important, as are their regulating cytokines IL-10 and IL-11. In terms of the nature of the inflammatory infiltrate, two apparently conflicting hypotheses have emerged: one based on direct observations of human lesions, the other based on animal experimentation and the inability to demonstrate IL-4 mRNA in gingival extracts. In the first of these, Th1 responses are responsible for the stable lesion, while in the second Th2 responses are considered protective. Using Porphyromonas gingivalis-specific T cell lines we have shown a tendency for IFN-gamma production rather than IL-4 or IL-10 when antigen is presented with peripheral blood mononuclear cells which may contain dendritic cells. It is likely that the nature of the antigen-presenting cell is fundamental in determining the nature of the cytokine profile, which may in turn open up possibilities for new therapeutic modalities.
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PMID:Cytokines in periodontal disease: where to from here? 1150 86

Interleukin (IL)-1alpha, IL-1beta, and IL-1ra contribute to regulation of the inflammatory response in periodontal tissues. We aimed to investigate the distribution of polymorphisms in the IL-1 gene family among periodontitis patients and controls, taking into account smoking and microbiology as additional variables. Fifty-three non-smoking and 52 smoking patients with severe adult periodontitis and 53 controls were genotyped for bi-allelic IL-1A(-889), IL-1B(-3954), and a penta-allelic 86-bp VNTR IL-1RN gene polymorphisms. The presence of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans was established by culture techniques. We found a higher frequency of allele 2 carriage in IL-1A, IL-1B, and IL-1RN in periodontitis patients who were non-smokers and in whom P. gingivalis and A. actinomycetemcomitans could not be detected (42.1% vs. 11.3% in controls; P = 0.0068; OR 5.7, 95% CI: 1.6-19.8). Our results provide evidence that polymorphisms in genes of the IL-1 family are associated with severe adult periodontitis in the absence of other risk factors tested in this patient population.
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PMID:Polymorphisms of the interleukin-1 gene family, oral microbial pathogens, and smoking in adult periodontitis. 1166 77

Several recent studies have investigated the association between interleukin-1 genotype and periodontitis in clinical samples, where generalizability is an issue. The aim of this study was to investigate the association between adult periodontitis and IL-1 genotype in a population-based sample of 26-year-olds. Based on probing depth (PD) measurements, participants were divided into three disease groups: "Severe" (1+ teeth with 5+mm PD; N = 25), "Moderate" (2+ teeth with 4+mm PD; N = 36), and "Controls" (the remainder; N = 800). The "periodontitis-associated genotype" (PAG; Kornman et al., 1997) was present in 20.0% of the "Severe" group and in 34.8% of "Controls", whereas the IL-1A(+4845) [1,1]/IL-1B(+3953) [2,2] genotype was present in 12.0% and 0.9%, respectively. After controlling for sex, smoking status, and plaque levels, we found that those with IL-1B(+3953) [1,1]/IL-1A(+4845) [2,2] had 12.3 times the odds of being in the "Severe" group. Analysis of these data suggests that the IL-1A(+4845) [1,1]/IL-1B(+3953) [2,2] genotype is associated with periodontal disease in this young population. Future periodontal data collections as this cohort ages are required to confirm the predictive value of that genotype.
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PMID:IL-1 genotype and adult periodontitis among young New Zealanders. 1166 78


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