UMLS:C0031099 - FACTA Search

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

The purpose of this pilot study was to evaluate the clinical and inflammatory changes produced in chronic, non-responsive periodontitis sites when comparing traditional scaling and root planing with scaling and root-planning using Perioscopy The sample size consisted of six patients who exhibited chronic periodontitis after completing initial therapy and under going periodontal maintenance for at least one year. The study was a within patient match site design. In which each patient had six to eight periodontal pockets measuring 5 mm to 8 mm. Half of the sites in each patients mouth were treated with scaling and root planing only (control group) and the other half of the sites were treated with scaling and root planing plus Perioscopy (experimental group). At one month evaluations, 50% of the control sites had a decrease of > 2 mm (11 out of 22 sites) and 55% of the experimental sites had a decrease in pocket depth of > 2 mm (12 out of 22 sites). When comparisons were made between baseline and three month evaluations of total pocket depths, 55% of the control sites had a decrease of > 2 mm (10 out of 22 sites). Chi-Square statistical analysis at one and three month evaluations showed non-significant decreases in pocket depth among control sites and experimental sites (p = 0.76, p = 0.55). At baseline, IL-1 mean levels and control sites were 43.47 pg/ml and 37.29 pg/ml for experimental for one month evaluation. II-1_mean levels were 33.03 pg/ml for control sites and 32.29 pg/ml for experimental sites. At the three month evaluation. IL-1 mean levels were 15.33 pg/ml for control sites and 14.42 pg/ml for experimental sites. Statistical t-test analysis assuming unequal variances at baseline, months one and three showed non-significant trends between control and experimental sites (p = 0.27, p = 0.47, p = 0.45). At baseline, PGE2, levels were 18.85 pg/ml for the control group abd 24,013 pg/ml for experimental sites. At one moth, PGE2 levels were 15.16 pg/ml for control sites and 16.23 pg/ml for experimental sites. At the three month evaluation, PGE2 levels were 14.18 pg/ml for the control sites and 15.92 pg/ml for the experimental group. T-test analysis of unequal variance showed non-significant trends in the data at baseline, one and three months for PGE2 (p = 0.26, p = 0.40, p = 0.31). The intent of this pilot study was to compare the changes in periodontal pocket depths and inflammatory markers of the control (scaling and root planing) and experimental (scaling and root planing with Perioscopy) sites. Analysis revealed no statistically significant differences in clinical and inflammatory analysis of the control sites and experimental sites though the three month evaluation period. Further studies are needed to determine the effectiveness of Perioscopy with a longer evaluation period.
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PMID:Clinical and inflammatory evaluation of Perioscopy on patients with chronic periodontitis. 1507 52

Several studies have shown a role for the involvement of interleukin (IL)-1 gene cluster polymorphisms in the risk of periodontal diseases. In the present study, we tested polymorphisms, derived from genes of the IL-1 cluster, for association with generalized aggressive periodontitis (GAP) through both allelic association and by constructing a linkage disequilibrium (LD) map of the 2q13-14 disease candidate region. The IL-1RN (VNTR) genotype distribution observed was significantly different in GAP and control subjects (P=0.019). We also observed some evidence for an association between GAP and the IL-1B(+3953) polymorphism (P=0.039). The pattern of association in the region, represented as an LD map, identifies a recombination hot area between the IL-1B(+3953) and IL-1B(-511) polymorphisms. Multilocus modelling of association with disease gives a location for the peak association at the IL-1B(+3953) marker, although support for the peak is not significant. Haplotype analysis identifies a IL-1B(+3953)-IL-1B(-511) haplotype as having the lowest P-value in the region. Recognition of the presence of a recombination hot area between the IL-1B(+3953) and IL-1B(-511) polymorphisms will have an important bearing on future efforts to develop higher resolution SNP analysis in this region for both this and other diseases for which this cluster is implicated.
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PMID:Linkage disequilibrium analysis of case-control data: an application to generalized aggressive periodontitis. 1560 86

Treponema maltophilum and Treponema lecithinolyticum belong to the group IV oral spirochetes and are associated with endodontic infections, as well as periodontitis. Recently, the genes encoding the major surface proteins (Msps) of these bacteria (MspA and MspTL, respectively) were cloned and sequenced. The amino acid sequences of these proteins showed significant similarity. In this study we analyzed the functional role of these homologous proteins in human monocytic THP-1 cells and primary cultured periodontal ligament (PDL) cells using recombinant proteins. The complete genes encoding MspA and MspTL without the signal sequence were cloned into Escherichia coli by using the expression vector pQE-30. Fusion proteins tagged with N-terminal hexahistidine (recombinant MspA [rMspA] and rMspTL) were obtained, and any possible contamination of the recombinant proteins with E. coli endotoxin was removed by using polymyxin B-agarose. Flow cytometry showed that rMspA and rMspTL upregulated the expression of intercellular adhesion molecule 1 (ICAM-1) in both THP-1 and PDL cells. Expression of proinflammatory cytokines, such as interleukin-6 (IL-6) and IL-8, was also induced significantly in both cell types by the Msps, as determined by reverse transcription-PCR and an enzyme-linked immunosorbent assay, whereas IL-1beta synthesis could be detected only in the THP-1 cells. The upregulation of ICAM-1, IL-6, and IL-8 was completely inhibited by pretreating the cells with an NF-kappaB activation inhibitor, l-1-tosylamido-2-phenylethyl chloromethyl ketone. This suggests involvement of NF-kappaB activation. The increased ICAM-1 and IL-8 expression in the THP-1 cells obtained with rMsps was not inhibited in the presence of the IL-1 receptor antagonist (IL-1ra), a natural inhibitor of IL-1. Our results show that the Msps of the group IV oral spirochetes may play an important role in amplifying the local immune response by continuous inflammatory cell recruitment and retention at an infection site by stimulation of expression of ICAM-1 and proinflammatory cytokines.
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PMID:Upregulation of intercellular adhesion molecule 1 and proinflammatory cytokines by the major surface proteins of Treponema maltophilum and Treponema lecithinolyticum, the phylogenetic group IV oral spirochetes associated with periodontitis and endodontic infections. 1561 63

Actinobacillus actinomycetemcomitans is implicated in the pathogenesis of localized aggressive periodontitis, and has the capacity to express a cytolethal distending toxin (Cdt). Gingival fibroblasts (GF) are resident cells of the periodontium, which can express several osteolytic cytokines. The aims of this study were a) to investigate the role of Cdt in A. actinomycetemcomitans-induced expression of osteolytic cytokines and their cognate receptors in GF and b) to determine if the previously demonstrated induction of receptor activator of NFkappaB ligand (RANKL) by A. actinomycetemcomitans is mediated by these pro-inflammatory cytokines or by prostaglandin E(2) (PGE(2)). A. actinomycetemcomitans clearly induced interleukin (IL)-6, IL-1beta, and to a minimal extent, tumor necrosis factor (TNF)-alpha mRNA expression. At the protein level, IL-6 but not IL-1beta or TNF-alpha expression was stimulated. The mRNA expression of the different receptor subtypes recognizing IL-6, IL-1beta and TNF-alpha was not affected. A cdt-knockout strain of A. actinomycetemcomitans had similar effects on cytokine and cytokine receptor mRNA expression, compared to its parental wild-type strain. Purified Cdt stimulated IL-6, but not IL-1beta or TNF-alpha protein biosynthesis. Antibodies neutralizing IL-6, IL-1 or TNF-alpha, and the PGE(2) synthesis inhibitor indomethacin, did not affect A. actinomycetemcomitans-induced RANKL expression. In conclusion, a) A. actinomycetemcomitans induces IL-6 production in GF by a mechanism largely independent of its Cdt and b) A. actinomycetemcomitans-induced RANKL expression in GF occurs independently of IL-1, IL-6, TNF-alpha, or PGE(2).
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PMID:Cytokine responses of human gingival fibroblasts to Actinobacillus actinomycetemcomitans cytolethal distending toxin. 1580 96

The aim of this retrospective study was to evaluate the influence of interleukin (IL)-1 genotype on the clinical parameters pocket probing depth and tooth loss in periodontally treated and regularly maintained patients. Only data from non-smokers were included. Patient mean data on pocket probing depth (PPD) and tooth loss from 53 Caucasian patients treated for generalized chronic periodontitis and maintained for an average of 15.5 years at the university of Kiel were analysed. All patients were genotyped and subjects with at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 were classified IL-1 genotype positive. 12 patients (22.6%) were IL-1 genotype positive. IL-1 genotype positive/negative patients were on average 46.3/45.8 years old with a mean of 23.8/23.9 teeth, resp., at baseline (TO). A total of 86 teeth were lost initially, resulting in an average of 21.5/ 22.5 teeth after active treatment (T1). The corresponding values after 13 years of supportive periodontal care (T2) were 20.7/21.6 teeth. Corresponding mean PPD values for IL-1 genotype positive/negative patients decreased from 4.7 mm/5.3 mm (To) to 2.9 mm/ 2.9 mm (T1) and increased slightly to 3.3 mm/3.4 mm at T2. Intergroup differences of PPD and tooth loss were not significant. Regarding pocket probing depth and tooth loss, there were no significant differences related to IL-1 genotype.
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PMID:Influence of interleukin (IL)-1 composite genotype on clinical variables in non-smoking, well-maintained compliant patients with chronic periodontitis. 1589 59

The aim of this paper was to review the relationship between periodontitis and preterm delivery (PTD). Original papers on this subject, published in English until the first quarter of 2004, were located in the MEDLINE/PubMed database. Additional papers were obtained by searching reference lists of previously published review papers. Case control studies pointed to an association between periodontitis and increased rates of PTD of low birth-weight (LBW) infants. Longitudinal studies showed that the incidence or progression of periodontitis during pregnancy may be an independent risk factor for PTD and LBW. Microbiological, immunological and animal model studies suggested that periodontal pathogens and their products may translocate to the fetal-placental unit resulting in PTD or fetal growth restriction. Maternal periodontal infection may also provide a chronic reservoir of inflammatory mediators and cytokines (TNF-alpha, IL-1, IL-6, PGE2) that could adversely affect pregnancy outcome. Randomized controlled studies published indicated that periodontal treatment significantly reduces the risk of PTD and LBW infants. If these results are confirmed in further intervention studies, then prevention and treatment of periodontitis should be considered as a necessary part of prenatal care.
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PMID:Periodontitis and preterm delivery. A review of the literature. 1590 58

Periodontitis, a chronic inflammatory disease, is characterized by increased expression of interleukin (IL)-1 and other inflammatory mediators resulting in extensive osteoclast formation and bone loss. Expression of receptor activator of nuclear factor kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), by osteoblasts is important to regulate osteoclast differentiation. The aim of the present study was to investigate the regulatory effects of IL-1 on RANKL and OPG production by mesenchymal fibroblasts in periodontal tissue. Human gingival fibroblasts (HGF) and periodontal ligament fibroblasts (PDL) were stimulated with IL-1alpha with or without protein synthesis inhibitor cycloheximide (CHX), protein kinase A (PKA) inhibitors, protein kinase C (PKC) inhibitors and prostaglandin E(2) (PGE(2)) inhibitor. In some experiments, the cultured cells were directly stimulated with either PKA or PKC activators. In HGF, IL-1alpha-stimulated OPG mRNA expression was high and could be reduced by CHX. PKA inhibitor completely abrogated IL-1alpha-induced OPG mRNA expression and OPG production. Endogenous PGE(2) further enhanced IL-1alpha-induced OPG production in HGF. In PDL, RANKL mRNA expression was greatly augmented by IL-1alpha. IL-1alpha induced OPG mRNA expression and protein production. PKC inhibitor partially reduced IL-1alpha-induced OPG production and PKC activator enhanced OPG production in PDL. The IL-1alpha-stimulated OPG mRNA expression in HGF was greater than PDL. These results provide new evidence for the possible osteoclastogenesis-inhibitory function of HGF through PKA activity pathway. PDL utilized PKC for OPG production. Thus, we emphasize that HGF and PDL have different characteristics of host defence mechanism against inflammatory process.
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PMID:Protein kinase-A-dependent osteoprotegerin production on interleukin-1 stimulation in human gingival fibroblasts is distinct from periodontal ligament fibroblasts. 1629 61

Inflammation plays a central role in many diseases of aging, and genetic differences in the inflammatory response appear to influence different disease courses among individuals. Variations in the genes for the family of interleukin 1 (IL-1) proteins are inherited together in a small set of patterns and provide an example of the role of inflammatory genetics as a modifier of diseases of aging. The IL-1 genetic variations are associated with variation in both the inflammatory response and the clinical presentation of a range of diseases, including coronary artery disease, Alzheimer disease, gastric cancer, and periodontitis. This growing understanding of the role of genetic variation in inflammation and chronic disease presents opportunities to identify healthy persons who are at increased risk of disease and to potentially modify the trajectory of disease to prolong healthy aging. Nutrition represents one of the promising approaches to modulation of the risk of diseases of aging because of the effects of certain nutrients on gene expression. One of the most practical applications of nutritional modulation of chronic disease may be nutrients that regulate the expression of key inflammatory genes.
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PMID:Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging. 1647 16

The aim of the present study was to determine the effects of meloxicam after initial periodontal treatment on interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1ra) in gingival crevicular fluid (GCF) and clinical parameters in the chronic periodontitis patients. Data were obtained from 30 patients with chronic periodontitis. Fifteen chronic periodontitis patients received 7.5 mg meloxicam, and 15 patients received placebo tablets in a 1x1 regimen for 1 month. All subjects were nonsmokers and had not received any periodontal therapy. The plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) were recorded. The GCF was collected using a paper strip: eluted and enzyme-linked immunoabsorbent assays (ELISAs) were performed to determine the cytokine levels. The clinical data and GCF samples were obtained after periodontal therapy and 1 month after periodontal therapy. The PI, GI, PD, and GCF IL-1ra decreased significantly (p<0.05) in meloxicam group at first month when comparing the initial levels. While decrease of the PI was statistically significant in control group (p<0.05), statistically significant changes were not determined in the other clinical parameters and GCF cytokine levels (p>0.05). There were no significant differences between two groups in any of the investigated parameters. Our observations did not reveal any influence of meloxicam on levels of IL-1beta and IL-1ra in chronic periodontitis. Additional clinical studies are advisable to determine whether COX-2 selective drugs alter periodontal disease outcome with greater safety.
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PMID:Effect of meloxicam on gingival crevicular fluid IL-1beta and IL1 receptor antagonist levels in subjects with chronic periodontitis, and its effects on clinical parameters. 1689 36

A genotype in the IL-1 gene cluster is associated with an increased risk of periodontitis. We investigated whether polymorphisms in the IL-1A +4845 and IL-1B +3954 loci affect the periodontal status of HIV-infected Brazilians on HAART. HIV-positive and HIV-negative subjects with periodontitis were genotyped for IL-1 by polymerase chain reaction and restriction enzyme digestion. Only 11.4% of patients were genotype positive. No associations between genotype positivity and HIV infection or periodontal status were found in this population.
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PMID:IL-1 gene polymorphism and periodontal status of HIV Brazilians on highly active antiretroviral therapy. 1693 44

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