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)

The purpose of this study was to assess the prognostic value of the IL-1 haplotype on the progression of periodontal disease following therapy. 48 adult patients with untreated periodontitis harboring Actinobacillus actinomycetemcomitans and/or Porphyromonas gingivalis were randomly assigned to receive full-mouth scaling alone (control) or in combination with systemic metronidazole plus amoxicillin and supragingival irrigation with chlorhexidine digluconate (test). All patients received supportive periodontal therapy at 3 to 6 months intervals. In 33 patients, lymphocyte DNA was analyzed for polymorphism in the IL-1A gene at position -889 and IL-1B gene at position +3953. Overall, 16 of 33 patients (7 of 17 test and 9 of 16 control) carried the IL-1 haplotype. 2 years following initial periodontal therapy, no differences in the survival rates of sites or teeth not exhibiting probing attachment loss of 2 mm or more compared to baseline, were found between patients who tested positive (85% sites, 53% teeth) and patients who tested negative (89% sites, 56% teeth) for the IL-1 haplotype. The results indicated that the IL-1 haplotype may be of limited value for the prognosis of periodontal disease progression following non-surgical periodontal therapy.
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PMID:Interleukin-1 haplotype and periodontal disease progression following therapy. 1059 9

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.
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PMID:Interleukin-1 genotypes and the association between periodontitis and cardiovascular disease. 1068 60

Bleeding on probing (BOP) is the most significant clinical parameter for the assessment of periodontal inflammation. The aim of this prospective longitudinal trial was to study the association between allelic variants of the IL-1 gene complex and gingival inflammation. Three hundred and twenty-three randomly selected periodontal maintenance patients (64.4% females) received a periodontal examination that included probing depth measurements and BOP at each of 4 supportive periodontal therapy (SPT) appointments. A blood sample taken from each subject was analysed for the presence of specific allotypes of the IL-1 gene complex. Two polymorphisms located at +4845 bp in the IL-1 alpha region and at +3954 bp in the IL-1 beta region were evaluated by a polymerase chain reaction method; 35.3% of the examined subjects were positive for specific combinations of allotypes of the IL-1 gene complex previously associated with an increased risk for severe periodontitis. The population consisted of 90 current smokers and 94 former smokers. An analysis of the association between the IL-1 genotype and BOP in the whole population (including smokers) did not reach statistical significance because of the overriding effect of smoking. A subset analysis of the 139 never smokers indicated that genotype positive patients had a significantly elevated chance of presenting an increase in the BOP% over a 4-appointment recall period (p = 0.03) after correcting for oral hygiene. In fact, patients who were genotype-negative had a 50% smaller chance of showing increases in BOP% during SPT. A further analysis explored the relationship between the genotype and the level of BOP% at the most recent recall visit. A generalized linear model showed a statistically significant effect of the genotype status after correcting for plaque accumulation and prevalence of residual pockets (> or = 5 mm). Genotype-negative subjects had significantly lower BOP% (p = 0.0097). It is concluded that the increased BOP prevalence and incidence observed in IL-1 genotype-positive subjects indicates that some individuals have a genetically determined hyper-inflammatory response that is expressed in the clinical response of the periodontal tissues.
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PMID:Effect of interleukin-1 gene polymorphisms on gingival inflammation assessed by bleeding on probing in a periodontal maintenance population. 1086 64

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

Factors which increase the risk of severe adult periodontitis (AP) may also contribute to the success of dental implants. To determine which cytokines may be relevant, levels of interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta), interleukin-1 receptor antagonist (IL-1ra), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) mRNA were quantitated in gingival tissue from periodontitis patients and healthy controls. Periodontitis significantly increased levels of IL-1alpha, IL-1beta, IL-6 and IFN-gamma mRNA relative to healthy tissues. IL-1 was selected for further study, as it has inflammatory and bone resorbing properties. We examined IL-1A(-889) and IL-1B(+3953) alleles in Caucasian patients with AP and early-onset periodontitis (EOP), patients with dental implants and healthy individuals. The IL-1B(+3953) polymorphism was associated with AP. This was evident from an increased homozygosity for allele 2 in patients with AP and a decreased heterozygosity in advanced AP patients. IL-1A(-889) and a composite genotype [IL-1A(-889)2 plus IL-1B(+3953)2] showed no association with the incidence of periodontitis, disease onset or disease severity. IL-1A(-889), IL-1B(+3953) and the composite genotype also showed no association with failure of dental implants.
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PMID:Do interleukin-1 polymorphisms predict the development of periodontitis or the success of dental implants? 1185 58

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.
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PMID:Periodontitis and diabetes interrelationships: role of inflammation. 1188 55

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions.
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PMID:Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research. 1188 56

Interleukin (IL)-1 alpha, IL-1 beta and IL-1 receptor antagonist (ra) play a major role in regulation of the inflammatory response in periodontal tissues. The aim of this study was to investigate the distribution of genetic variation in the IL-1 gene family among periodontitis patients and controls, taking into account smoking and microbiology as additional variables. There were 53 non-smoking and 52 smoking patients with severe adult periodontitis and 53 periodontal healthy controls genotyped for genetic variation in the IL-1 gene family. The presence of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans was established by culture techniques. A higher frequency of genotype+ (IL-1A*2 + IL-1B*2 + IL-1RN*2) was found in non-smoking periodontitis patients 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). This data provide evidence that polymorphisms in genes of the IL-1 family are associated with severe adult periodontitis and may be a risk factor for severe periodontitis.
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PMID:[Risk factors in adult periodontitis: polymorphism in the interleukin-1 gene family]. 1221 56

Keratinocyte growth factor (KGF) and hepatocyte growth factor/scatter factor (SF) are two signalling molecules thought to play important roles in regulating epithelial-mesenchymal interactions. Expression of both factors by fibroblasts in subepithelial connective tissue may play a role in maintaining epithelial integrity in health and in the apical migration of junctional epithelium in periodontitis. The aims of this study were (a) to compare expression levels of KGF and SF by periodontal ligament (PDL) and gingival fibroblasts; and (ii) to determine the effects of interleukin (IL)-1 beta, transforming growth factor (TGF)-beta 1, platelet-derived growth factor (PDGF)-BB and epidermal growth factor (EGF) on KGF/SF expression by these cell populations. Three paired PDL and gingival fibroblast strains were developed. The KGF and SF protein levels were analysed by enzyme-linked immunosorbent assay. Relative levels of KGF and SF mRNA in cytokine-treated cultures were determined using semiquantitative reverse transcriptase polymerase chain reaction. No differences in the levels of KGF and SF produced by PDL and gingival (SOG) populations were found. In both cell types IL-1 beta stimulated KGF and SF expression, while TGF-beta 1 significantly inhibited expression at both the mRNA and protein levels. Epidermal growth factor and PDGF-BB induced differing effects on expression, stimulating SF protein production but inhibiting KGF output in both fibroblast populations. Differences in response to EGF and PDGF were also seen between paired PDL and gingival fibroblasts.
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PMID:Keratinocyte growth factor and scatter factor expression by regionally defined oral fibroblasts. 1255 7


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