UMLS:C0031099 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

Periodontitis is a general term for disease categories, including juvenile periodontitis (JP), rapidly progressive periodontitis (RPP), and adult periodontitis (AP), which may or may not share a common etiology and pathogenesis. These disease categories are characterized by differences in progression of tissue destruction and differences in age group susceptibility, but not, to our knowledge, by differences in cytokine responses of inflammatory cells. The present study examined blood cell counts and interindividual variation in the ability of PBMC of patients in three different categories of periodontitis to produce cytokines after stimulation with different oral bacterial species in vitro. The AP group had a significantly lower production of IL-1ra when stimulated with Porphyromonas gingivalis (P.g.) and Actinobacillus actinomycetemcomitans (A.a.) (P < 0.05). Streptococcus sanguis (S.s.), which is associated with normal periodontal conditions, induced extremely high levels of IL-1 alpha and TNF alpha production in all groups. The RPP group had a significantly higher number of monocytes (MC) than the AP group (P < 0.05). Additionally, JP patients had a significantly higher concentration of polymorphonuclear granulocytes compared to juvenile controls (P < 0.05). In conclusion, IL-1 alpha, TNF alpha, or IL-6 production by peripheral blood MC after in vitro stimulation with oral bacterial type stains may not distinguish different categories of periodontitis. The results support the hypothesis that the cytokine IL-1ra is produced in different concentrations in the two groups: RPP and AP. Furthermore, elevated MC concentration in the RPP group compared to the AP group may be an important pathogenic feature in RPP.
...
PMID:Bacterial-stimulated cytokine production of peripheral mononuclear cells from patients of various periodontitis categories. 773 Sep 65

Chronic inflammation induced by bacteria often leads to host-mediated destruction of tissues adjacent to the sites of microbial insult. The chronic inflammatory process of adult periodontitis results in the destruction of supporting osseous and connective tissues of the teeth. We hypothesized that virulence factors of periodontal pathogens such as lipopolysaccharide stimulate inflammatory cytokine expression by mononuclear cells of the host which contribute to disease development. In this study, to elucidate the role of these cytokines in chronic adult periodontitis, we tested whether the prevalence of mRNA for inflammatory cytokines generally associated with mononuclear phagocytes was higher in diseased than in healthy gingival tissue. Gingival mononuclear cells or whole gingival biopsies from 32 adult periodontitis patients and five healthy individuals used as controls were evaluated for inflammatory cytokine mRNA expression by reverse-transcription polymerase chain-reaction (RT-PCR) procedures. The cytokines assessed included IL-1 alpha, IL-1 beta, IL-1ra, IL-6, IL-8, IL-12, IL-13, TNF-alpha, TGF-beta, and IFN-gamma. The monocyte/macrophage lipopolysaccharide (LPS) receptor CD14 was also assessed. Results showed that TNF-alpha mRNA was present significantly more frequently in diseased than in healthy biopsies, whereas IL-1 alpha, IL-1 beta, and IL-1ra mRNA were found in most (from 80 to 100%) healthy tissues. Message for CD14 was present in both healthy and diseased tissue samples (100%). This study provides evidence for a major role of TNF-alpha in chronic adult periodontitis. Moreover, our results suggest that the mononuclear cells derived from periodontal tissues have the capacity to respond to components of periodontal pathogens and express both pro- and anti-inflammatory cytokines in these tissues.
...
PMID:Profile of cytokine mRNA expression in chronic adult periodontitis. 939 Apr 76

Adult periodontitis is a chronic destructive disease characterized by an interaction between gram-negative bacteria and the host inflammatory response. Microbial substances such as lipopolysaccharide can activate host cells, e.g., macrophages, fibroblasts and keratinocytes, to secrete proinflammatory cytokines including tumor necrosis factor alpha and interleukin 1 beta (IL-1 beta). This study examined the hypothesis that periodontitis tissue contains increased levels of cytokines that promote osseous and connective tissue destruction. To test this hypothesis, diseased and healthy gingival biopsies were examined for differences in the expression of cytokine mRNA for the pro-inflammatory cytokines tumor necrosis factor alpha and IL-1 beta and the anti-inflammatory cytokine IL-1ra using quantitative reverse transcriptase polymerase chain reaction and in situ hybridization methods. The levels of tumor necrosis factor alpha and IL-1ra mRNA were shown to be significantly higher in diseased than healthy tissues. Additionally, a significantly correlated expression of IL-1 beta and IL-1ra mRNA was seen in all tissue examined. Analysis of tissue sections by immunohistochemical and in situ hybridization techniques revealed a mononuclear cell infiltrate that consisted of a higher average number of cells staining positive for tumor necrosis factor alpha mRNA, CD14, and CD3 in the diseased than healthy tissues. Although both diseased and healthy tissues expressed IL-1 beta and IL-1ra mRNA in the epithelium, the diseased tissue biopsies expressed more IL-1 beta and IL-1ra mRNA in the connective tissue. These results implicate the potential involvement of both the pro- and anti-inflammatory cytokines in the regulation of the chronic inflammatory disease adult periodontitis.
...
PMID:Quantitative assessment of inflammatory cytokine gene expression in chronic adult periodontitis. 957 7

An epidemiological association between periodontitis and cardiovascular disease has been reported in multiple studies. Various mechanisms have been proposed as potential explanations for this association, including a common factor that predisposes certain individuals to a hyper-responsive inflammatory response. Variations in the genes that regulate the interleukin-1 (IL-1) response have been associated with both periodontal disease and cardiovascular disease. New data indicate that one pattern of IL-1 genetic polymorphisms, characterized by the IL-1A (+4845) and IL-1B (+3954) markers, is associated with periodontitis but not certain measures of atherosclerosis. Another IL-1 genetic pattern, characterized by the IL-1B (-511) and IL-1RN (+2018) markers, is associated with atherosclerotic plaque formation, as measured by angiography and arterial wall thickness, but not periodontitis. These two patterns also have different functional implications relative to IL-1 biological activity. Studies of IL-1 gene polymorphisms, atherosclerotic plaque instability and cardiovascular clinical events are in progress. Hypothetical models are presented to explain how IL-1 genetic factors may be involved in cardiovascular disease.
...
PMID:Interleukin-1 genotypes and the association between periodontitis and cardiovascular disease. 1068 60

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.
...
PMID:Polymorphisms of the interleukin-1 gene family, oral microbial pathogens, and smoking in adult periodontitis. 1166 77

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.
...
PMID:Linkage disequilibrium analysis of case-control data: an application to generalized aggressive periodontitis. 1560 86

Genetic variants at multiple loci have been shown to be associated with periodontitis risk. In this study, we have focused on nine functional gene polymorphisms encoding immunoregulation-related molecules such as cytokines (interleukin-1 (IL-1), transforming growth factor-beta1 (TGF-beta1)) and cell surface receptors (immunoglobulin G and A Fc receptors (Fc gamma R and Fc alpha R)). In total, 113 Japanese patients with chronic periodontitis (CP) and 108 race-matched healthy controls were genotyped with the modified serial invasive signal amplification reaction. There was a significant difference in the distribution of IL-1 receptor antagonist (RN) +2018 T/C allele between the patient and control groups, with enrichment of the +2018 C in controls (P = 0.021, odds ratio = 0.38). An increased frequency of the IL-1 haplotype comprising IL-1A +4845 G, IL-1B -31 C, and IL-1RN +2018 C was observed in controls (P = 0.004). Moreover, a multivariate logistic regression analysis revealed that subjects with IL-1RN +2018 C allele were less likely to have CP (P = 0.016, odds ratio = 0.29). These findings document the association of IL-1RN +2018 C with reduced susceptibility to CP in the Japanese.
...
PMID:Association of interleukin-1 receptor antagonist +2018 gene polymorphism with Japanese chronic periodontitis patients using a novel genotyping method. 1832 9

The aim of this work was the determination of the state of local immunity in periodontal complex in patients with chronic generalized periodontitis (CGP). 96 individuals were examined (mean age 43.6+/-1.2 years). All the patients were divided into 2 groups: basic group with CGP patients (76 persons) and comparative group - individuals with intact periodontium (20 persons). To evaluate local immunity in dentogingival fluids the determination of concentrations of IgG, IgM, and IgA immunoglobulins has been used, as well as TNF-alpha, IL-1, IL-6, IL-8, INF-gamma, IL-1ra, IL-10, and IL-4 cytokines, and also factors controlling the state of bone tissue, namely, osteoprotegerine (OPG), and RANK-ligand. In gingival fluid of CGP patients the increase in both pro-, and anti-inflammatory mediators with indication to Th2-deviation (decrease of INF-gamma level and elevation of IL-4 level) was observed. CGP patients exhibited in their periodontal complex marked increase of IgG, IgM, and IgA concentrations that apparently evidenced to the consequence of local polyclonal activation of B-lymphocytes. Gingival fluid of CGP patients showed the elevation of RANKL, TNF-alpha, and IL-1 levels, and the decrease in OPG concentration that could be the reason for osteoclast activation and subsequent destruction of bone tissue. In case of CGP in the zone of periodontium developed <<atypical>> inflammation that is characterized by elevated level of IL-8 and predominance of neutrophil number over the quantity of other types of leukocytes.
...
PMID:[State of local immunity in patients with chronic generalized parodontitis]. 1883 35

There is no doubt that plaque bacteria are necessary to initiate disease and drive the chronic inflammatory response in the periodontal tissues. At the same time, there is strong evidence that destructive processes occurring as part of the host inflammatory response are responsible for the majority of the hard- and soft-tissue breakdown leading to the clinical signs of periodontitis. The characteristic clinical signs of chronic periodontitis occur mainly as a result of activation of host-derived immune and inflammatory defense mechanism. IL-1 and TNF induce expression of other mediators that amplify the inflammatory response, such as prostaglandins, and lead to production of lytic enzymes and stimulate the production of chemokines. Investigations on the soluble protein delivery of antagonists to IL-1 and TNF in animal models have shown promising results. Collectively, the clinical, radiographic, and biochemical findings of these experiments show that IL-1 and TNF-alpha antagonists block the progression of the inflammatory cell infiltrate towards the alveolar crest and the recruitment of osteoclasts, and prevent the periodontal lesions may destroy the soluble cytokine antagonists prior to their peak activity, which may necessitate more frequent administration of the active agents to the defects. Thus, gene transfer of TNF receptor antagonists and IL-1ra may offer a more efficient mode of delivery of disease controlling agents to the periodontal structures. Periodontal treatment through the ages has focused on the reduction of bacterial infection by mechanical removal of infectious agents (i.e., SRP). Attempts at elimination of infectious agents often do not represent a definitive therapy in periodontitis, necessitating the administration of more sophisticated biological treatment modalities. A thorough understanding of the host inflammatory response in periodontal pathogenesis presents the opportunity for exploiting new treatment strategies for periodontitis by means of host response modulation. The rationale behind this approach is to aid the host in its fight against infectious agents by supplementing the natural inherent defense mechanism or to modify its responses by changing the course of inflammatory systems. Therefore, pharmaceutical inhibition of host response pathways that mimic endogenous anti-inflammatory mechanisms may prove to be an effective strategy for treating periodontal diseases. This would require the development of polypharmaceutical approaches controlling all pathways associated with inflammation and tissue destruction. Current research has focused on the use of SDD as a treatment modality, and SDD is the only systemically used host modulatory drug approved by the United States Food and Drug Administration.
...
PMID:Pathogenesis of periodontitis: role of cytokines in host response. 2097 18

This study examined the association of IL1 genetic polymorphisms (IL-1A +4845, IL-1B +3954 & IL-1RN +2018) with periodontal disease status of Down syndrome (DS) individuals. Fifty-four DS patients (18-56 yr, 48.15% male, 77.78% Caucasians) were recruited from the Georgia Regional Hospital (GRH) health care system. Two comparable groups (71 mentally retarded patients and 87 control subjects) were also recruited. All subjects were nonsmokers. Periodontal evaluations (plaque index, gingival index, bleeding-on probing and clinical attachment levels (AL)), personal and professional dental care habits were recorded. Blood was collected by a venipuncture. The IL-1A +4845, IL-1B +3954 & IL-1RN +2018 loci were genotyped by the TaqMan assay. No statistically significant differences were noted in the distribution of IL-1 gene polymorphisms between the three groups. The IL-1 variant genotypes varied by race; for both IL-1A and IL-1RN, the variant gene was significantly more prevalent among whites than non-whites (ps > 0.1). ANCOVA, which also adjusted for age, showed a 3-way interaction among dental visits, gene variation and Down status [(F(1, 179) = 3.96, P = 0.048 in White subjects and F(1, 241) = 2.96, P = 0.087 in all subjects). Post-hoc t-tests confirmed lower levels of AL in IL-1RN-variant Down subjects receiving more frequent dental visits (P < 0.05). ANCOVA, which also adjusted for age, showed an interaction between IL-1A/B gene variation and Down status (F(1, 174) = 3.04, P = 0.083 in White subjects and F(1, 235) = 3.72, P = 0.055 in all subjects). Post-hoc t-tests confirmed lower levels of AL in IL-1A/B-variant Down subjects (P < 0.05). The distribution of variant IL-1 genes in DS subjects was not different from the general population. However the association between the carriage of the IL-1 rare alleles and periodontitis differed between the Down and non-Down subjects. The carriage of the IL-1 rare alleles in the Down subjects tended to confer a protective effect against loss of periodontal attachment.
...
PMID:Association of interleukin-1 polymorphisms with periodontitis in Down syndrome. 2171 24

1 2 Next >>