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)

A case of necrotizing ulcerative periodontitis (NUP), the most severe inflammatory periodontal disorder caused by plaque bacteria, is shown. Clinically, the gingiva showed distinct signs of ulceration, and radiography revealed horizontal bone loss. Indirect immunofluorescence, carried out on frozen sections of tissue specimens obtained from the NUP lesion, exhibited clear expression of atypical keratin K19, particularly in basal cells, when compared to noninflamed gingiva. Moreover, NUP tissue showed extensive intraepithelial abundance for the basement membrane component laminin-1/10 and the extracellular matrix molecule tenascin. Strong expression of integrin subunit alphav and matrix metalloproteinase-13 in conjunction with interleukin 1-beta further discriminated NUP gingival epithelium from normal tissue. The results suggest that NUP is associated with changes in the expression and topography of the analyzed molecules in the gingival epithelium, which in turn may reflect the fast progression of the disease.
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PMID:Molecular changes in the gingival epithelium associated with necrotizing ulcerative periodontitis: a case report. 1664 8

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

The researchers studied the polymorphism of IL-1alpha and Il-beta genes in patients of different ages with severe chronic generalized periodontitis and people with healthy periodontium. They used molecular and genetic techniques such as polymerase chain reaction and reverse hybridization with Geno Type PRT reagents (Germany). The study demonstrated a correlation between high frequency of genetic polymorphism in IL-1A -899 and IL-1B +3953 loci and the development of severe periodontitis in patients less than 35 years of age, and a possibility of using this parameter in complex assessment of patients with periodontal diseases. The research suggests that Geno TypeR PRT test system should be recommended for evaluation of patients with a high risk of aggressive periodontal diseases, as well as patients with therapy-resistant periodontitis.
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PMID:[The allelic polymorhism of IL-1alpha and IL-beta genes in patients with chronic inflammatory periodontal diseases]. 1750 Feb 14

Our 10-year study of early-onset periodontitis (EOP) patients includes repeated clinical observations, microbiological characteristics and analysis of genetic polymorphism of IL-1A and IL-1B genes. Twenty patients (age 15-26 years) were divided according to the clinical status in the 4th year into a group with mean number of teeth with bleeding on probing (BP) 9.8 and mean number of teeth with periodontal pocket (PP) 2.23, and a group with mean number of teeth with BP 5.37 and no PP. Significantly higher values of mean BP and PP were found among the groups during the study but a strong progression of disease was found only in 3 patients. The risk IL-1A allele-2 and IL-1B allele-2 genotype and bacterial presence were analyzed by DNA hybridization methods. No significant differences of bacteria composition (Treponema denticola, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans) were found between the groups. A higher prevalence of composite IL-1 genotype was detected in the group of EOP patients with progressive disease. Early finding of the disease followed by conservative therapy could positively influence the disease progression. EOP treated in early stages may, but need not, develop into the aggressive form in the presence of risk genotype IL-1.
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PMID:Interleukin- 1 gene polymorphisms as assessed in a 10-year study of patients with early-onset periodontitis. 1757 17

An increasing number of evidence supports the assumption that genetic factors have crucial role in the development of periodontitis and hypodontia. The strategic purpose of the authors is to identify the genetic background of these disorders and to map the gene polymorphisms involved in their development. As a first step of an experimental series, we aimed to set and optimize multiple individual gene polymorphism identification methods by the combination of polymerase chain reaction and restriction fragment length polymorphism analysis methods. We have successfully optimized eight single nucleotide polymorphism procedures that are potentially involved in periodontitis (IL-1 alpha -889, IL-1 beta -511, IL-1 beta +3954, IL-6 -174, IL-10 -1082, TLR-4 -299, TLR-4 -399, TNF-alpha -308), and another two that might be related to the appearance of hypodontia (PAX9 -1032, PAX9 -912). Besides the dominant allele, we also observed the presence of the rare allele in each polymorphism although at present we have a small sample number. These preliminary studies provide evidence for the feasibility of further investigations with large sample numbers comparing control and patient groups. These studies may lead to the development of new diagnostic strategies and provide novel tools for the early recognition of genetic predisposition and the primary control of the diseases. Furthermore, they project future therapeutic avenues for gene therapy in the cure and prevention of oral disorders.
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PMID:Gene polymorphisms in periodontitis and hypodontia: methodological basis of investigations. 1807 45

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.
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PMID:Association of interleukin-1 receptor antagonist +2018 gene polymorphism with Japanese chronic periodontitis patients using a novel genotyping method. 1832 9

Localized aggressive periodontitis (LAgP) is a complex multifactorial periodontal disease to which genetic factors are thought to predispose individuals. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are potent immunomodulators and proinflammatory cytokines that have been implicated in the pathogenesis of autoimmune and infectious diseases and proposed to be risk factors for LAgP. Our aim was to investigate IL-1 alpha (+4845), IL-1 beta (+3954), and TNF-alpha (-308) gene polymorphisms in Turkish LAgP patients. We genotyped 31 LAgP patients and 31 healthy controls for IL-1alpha(+4845), IL-1beta(+3954), and TNF-alpha(-308) using standard PCR amplification followed by restriction enzyme digestion and gel electrophoresis. Higher prevalence of heterozygosity for IL-1alpha(+4845) was found in cases (65%) when compared to controls (35%) (P < 0.05). While homozygous allele 1 of IL-1beta(+3954) was the most frequent genotype in cases (62%), no controls were homozygous for this allele (P < 0.001). Homozygous allele 1 was the most common TNF-alpha genotype in both groups, however no significant difference in TNF-alpha genotypes was found between groups. In conclusion, in this Turkish population, susceptibility to LAgP is increased by heterozygosity for allele 1 of IL-1alpha(+4845) or homozygosity for allele 1 of IL-1beta(R+3954). Moreover, IL-1 gene polymorphisms appear to have a role in susceptibility to LAgP, and the above-mentioned genotypes could be an important risk factor for LAgP in the Turkish population.
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PMID:Interleukin-1 and tumor necrosis factor-alpha gene polymorphisms in Turkish patients with localized aggressive periodontitis. 1858 4

The mitogen-activated protein (MAP) kinase phosphatase (MKP) family plays an important function in regulating the pro-inflammatory cytokines by deactivating MAP kinases. MKP-1 is essential for the dephosphorylation of p38 MAP kinase that regulates expression of IL-6, TNF-alpha, and IL-1 beta. We hypothesized that MKP-1 regulates inflammatory bone loss in experimental periodontitis. Wild-type and Mkp-1(-/-) mice received A. actinomycetemcomitans LPS injection in the palatal region or PBS control 3 times/wk for 30 days. Mice were killed, and maxillae were assessed by microcomputed tomography, histological analysis, and TRAP staining for measurement of bone loss, extent of inflammation, and degree of osteoclastogenesis. Results indicated that, in LPS-injected Mkp-1(-/-) mice, significantly greater bone loss occurred with more inflammatory infiltrate and a significant increase in osteoclastogenesis compared with Mkp-1(-/-) control sites or either wild-type group. Analysis of these data indicates that MKP-1 plays a key role in the regulation of inflammatory bone loss.
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PMID:MAP kinase phosphatase-1 protects against inflammatory bone loss. 1986 41

This study investigated the association of IL-1A (+4845) and IL-1B (+3954) gene polymorphism with the subgingival microbiota and periodontal status of HIV-infected Brazilian individuals on highly active antiretroviral therapy (HAART). One hundred and five subjects were included in the study, distributed into 2 HIV groups [29 chronic periodontitis (CP+) and 30 periodontally healthy (H+)]; and 2 non-HIV groups (29 CP- and 17 H- patients). IL-1A and B were genotyped by PCR and restriction enzyme digestion. Thirty-three bacterial species were detected by checkerboard. Overall, we observed a prevalence of the allele 2 in the IL1-A and IL-1B polymorphism at 30.5% and 25.7%, respectively. Only 11.4% of all patients were composite genotype-positive, and 75% of those were HIV-infected. No significant associations between polymorphism of the IL-1 gene and periodontitis or HIV infection were observed. Likewise, no significant differences in the frequency and counts of any bacterial species were found between individuals with and without allele 2 (IL-1A or IL-1B). The data indicated that the IL-1 gene polymorphism is neither associated with periodontal destruction nor with high levels of subgingival species, including putative periodontal pathogens in HIV Brazilian individuals on HAART.
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PMID:Influence of IL-1 gene polymorphism on the periodontal microbiota of HIV-infected Brazilian individuals. 2002 54

Tobacco smoking is the main risk factor associated with chronic periodontitis, but the mechanisms that underlie this relationship are largely unknown. Recent reports proposed that nicotine plays an important role in tobacco-related morbidity by acting through the nicotinic acetylcholine receptors (nAChRs) expressed by non-neuronal cells. The aim of this study was to investigate whether alpha 7 nAChR was expressed in periodontal tissues and whether it functions by regulating IL-1 beta in the process of periodontitis. In vitro, human periodontal ligament (PDL) cells were cultured with 10(-12) M of nicotine and/or 10(-9) M of alpha-bungarotoxin (alpha-Btx), a alpha 7 nAChR antagonist. The expression of alpha 7 nAChR and IL-1 beta in PDL cells and the effects of nicotine/alpha-Btx administration on their expression were explored. In vivo, an experimental periodontitis rat model was established, and the effects of nicotine/alpha-Btx administration on expression of alpha 7 nAChR and development of periodontitis were evaluated. We found that alpha 7 nAChR was present in human PDL cells and rat periodontal tissues. The expressions of alpha 7 nAChR and IL-1 beta were significantly increased by nicotine administration, whereas alpha-Btx treatment partially suppressed these effects. This study was the first to demonstrate the functional expression of alpha 7 nAChR in human PDL cells and rat periodontal tissues. Our results may be pertinent to a better understanding of the relationships among smoking, nicotine, and periodontitis.
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PMID:Functional expression of alpha 7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues. 2030 83


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