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

The development of an assay for markers of active periodontitis, obtained directly from gingival crevicular fluid (GCF) and simply quantified, would be of great importance to the dental practitioner. The purpose of this study was to evaluate direct and indirect immunodot techniques as to their potential in easily quantifying acute-phase proteins within periodontally diseased and healthy site GCF. Indirect immunodots (GCF eluates dotted onto nitrocellulose membrane) using monoclonal antibodies and a radioactive isotope label were used to identify and establish relative amounts of C-reactive protein (CRP) and alpha-2-macroglobulin (A2M) in 2 diseased and 2 healthy sites in 24 periodontitis patients. Periodontally diseased sites were found to contain significantly lower concentrations of A2M than healthy sites (p less than 0.001), but CRP levels did not vary significantly between healthy and diseased locations. Using a direct immunodot assay (GCF absorbed directly into nitrocellulose membrane strips), A2M levels quantified with radioactive isotopes at healthy and diseased sites could be correlated with A2M levels determined by enzyme-linked antibody-colormetric probes at those same sites. Such a direct sampling and quantification system shows promise for future "in-office" diagnostic methodology.
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PMID:Acute-phase protein detection and quantification in gingival crevicular fluid by direct and indirect immunodot. 170 52

Pocket depth, attachment level (AL), bleeding on probing (BOP), amount of dental plaque and calculus, concentrations of immunoglobulin G and C-reactive protein in GCF were determined at 54 periodontal sites in 9 patients suffering from adult periodontitis before and 1 week after periodontal initial therapy (IT). At the same time the subgingival plaque was assessed by dark-field microscopy (DFM). 17% of the sites treated showed further loss of attachment. Attachment gain was observed at 39% of the examined sites. IT had no influence on the IgG- and CRP-concentrations of GCF. Measuring of AL, BOP and the assessment of subgingival plaque by DFM seem to be recommendable measures for monitoring adult periodontitis.
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PMID:[The influence of initial therapy on the symptoms of adult periodontitis]. 181 56

Five host-response indicators were measured by enzyme-linked immunosorbent assays on unstimulated whole saliva samples from 45 adults (19 male, 26 female). The participants were distributed among four dentate groups representing oral health (I), gingivitis (II), moderate periodontitis (III), and severe periodontitis (IV), and one group of edentulous volunteers (V). Levels of the host-response indicators varied widely, from zero, primarily with groups I and V, to relatively high values with groups II, III and IV. The levels ranged as follows: alpha 2-macroglobulin, 0-4941 ng/ml; alpha 1-antitrypsin, 2-2271 ng/ml; C-reactive protein, 0-472 pg/ml; cathepsin G, 0-6035 ng/ml; elastase, 0-164 ng/ml (free), 0-732 ng/ml (bound to alpha 1-antitrypsin), and 0-318 ng/ml (bound to alpha 2-macroglobulin). Statistical evaluation by planned contrasts showed that levels of host-response indicators for group I were significantly lower (except for alpha 1-antitrypsin) than for groups II, III, and IV. A trend analysis of groups I-IV showed that mean scores (again, except for alpha 1-antitrypsin) increased significantly in a positive, monotonic manner. Group V showed significantly lower values for elastase than in the other groups. The findings demonstrate that these factors can be detected in whole saliva and suggest that, except for alpha 1-antitrypsin, their levels are directly related to an individual's periodontal status.
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PMID:Salivary levels of alpha 2-macroglobulin, alpha 1-antitrypsin, C-reactive protein, cathepsin G and elastase in humans with or without destructive periodontal disease. 885 Jun 55

Capture ELISAs with biotinylated monospecific antibodies were developed to detect both C-reactive protein (CRP) and haptoglobin (Hp) in serum of adult periodontitis (AP) patients and normal subjects. Each acute-phase reactant was significantly increased in serum from AP patients with CRP at 9.12 +/- 1.61 mg/l versus 2.17 +/- 0.41 mg/l (P < 0.001) and Hp at 3.68 +/- 0.37 g/l versus 1.12 +/- 0.78 g/l (P < 0.001). Assessment of clinical characteristics of the patients' periodontal disease indicated that CRP and Hp levels were significantly increased in patients with the most frequent disease active episodes (P < 0.02 and P < 0.001, respectively). Longitudinal examination of the Hp levels showed a significant decrease following scaling and root planing (3.68 versus 2.38 g/l; P < 0.01). After a 2-year administration of 50 mg/b.i.d. Flurbiprofen (a non-steroidal anti-inflammatory drug), significantly decreased Hp levels were noted (P < 0.005). CRP levels declined by 35-40% after 1-2 years of treatment with the drug (P < 0.05). The findings indicated that localized infections resulting in increased inflammation and tissue loss in the periodontium elicit systemic host changes manifest by increases in two acute-phase reactants. The conclusions are that either these molecules are formed locally and distributed to the serum, or these presumably localized infections impact upon the systemic components of the host protective responses.
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PMID:Systemic acute-phase reactants, C-reactive protein and haptoglobin, in adult periodontitis. 903 Aug 74

Rapidly progressive periodontitis (RPP) results from the interaction between the periodontal microflora and the host. Stress is believed to play an important role in determining host responses, and it has been proposed that hyperactivity of host defense mechanisms significantly increases tissue destruction typical for this disease. During a period of four months we have diagnosed 20 patients with acute RPP, all of them active participants in battles of the Croatian liberation war with posttraumatic stress disorder (PTSD) related symptoms. In these patients we analyzed biochemical parameters in unstimulated saliva and performed microbiological analyses of periodontal pockets. These findings were compared with those of patients with adult periodontitis (AP), edentulous and healthy persons, none of whom participated in the war. Persons with AP had reduced concentrations of host humoral defense factors in saliva (C-reactive protein, C3 component of complement, and aplha alpha 2-macroglobulin), while patients with RPP had increased concentration of interleukin-6 (IL-6). IL-6 is released by host inflammatory cells and is a mediator of bone resorption. Actinobacillus actinomycetemcommitans and Peptostreptococcus were more frequently isolated from patients with RPP. We interpret these results as indicators of the importance of stress in the causation of RPP, with host inflammatory hyperactivity playing an important role in tissue destruction, specially alveolar bone resorption possibly caused by increased local levels of IL-6.
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PMID:Inflammatory mediators in saliva of patients with rapidly progressive periodontitis during war stress induced incidence increase. 1040 13

Periodontitis, a consequence of persistent bacterial infection and chronic inflammation, has been suggested to predict coronary heart disease (CHD). The aim of this study was to investigate the impact of periodontitis on HDL structure and antiatherogenic function in cholesterol efflux in vitro. HDL was isolated from 30 patients (age 43.6 +/- 6.1 years, mean +/- SD) with periodontitis before and after (3.2 +/- 1.4 months) periodontal treatment. The capacity of HDL for cholesterol efflux from macrophages (RAW 264.7), HDL composition, and key proteins of HDL metabolism were determined. After periodontal treatment, phospholipid transfer protein (PLTP) activity was 6.2% (P<0.05) lower, and serum HDL cholesterol concentration, PLTP mass, and cholesteryl ester transfer protein activity were 10.7% (P<0.001), 7.1% (P=0.078), and 19.4% (P<0.001) higher, respectively. The mean HDL2/HDL3 ratio increased from 2.16 +/- 0.87 to 3.56 +/- 0.48 (P<0.05). HDL total phospholipid mass and sphingomyelin-phosphatidylcholine ratio were 7.4% (P<0.05) and 36.8% (P<0.001) higher, respectively. The HDL-mediated cholesterol efflux tended to be higher after periodontal treatment; interestingly, this increase was significant (P<0.05) among patients whose C-reactive protein decreased (53.7% reduction, P=0.015) and who were positive by PCR for Actinobacillus actinomycetemcomitans. These results suggest that periodontitis causes similar, but milder, changes in HDL metabolism than those that occur during the acute-phase response and that periodontitis may diminish the antiatherogenic potency of HDL, thus increasing the risk for CHD.
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PMID:Periodontitis decreases the antiatherogenic potency of high density lipoprotein. 1313 Jan 23

Cardiovascular diseases and infections remain the first mortality causes in ESRD patients. European recommendations for good clinical practice in the hemodialysis field advocate to use the inflammation markers in daily practice. These markers foretell both cardiovascular and global mortality. They also enable to detect the silent infections (parodontitis, Heliobacter pilory infection, shunt infection in PTFE), to make sure of the dialysis biocompatibility (microbiological quality of the dialysate, use of biocompatible membrane). The C-reactive protein is the most current and used marker. Its use, combined with the procalcitonin measurement, specific marker for bacterial infection, would enable the diagnostic and therapeutic strategy improvement.
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PMID:[Inflammation markers in daily practice]. 1465 Jul 45

We investigated the relationship between periodontitis and mortality in home-dwelling individuals aged (75+ years), considering potential confounders including C-reactive protein levels. This study involved 364 individuals, originally part of the Helsinki Ageing Study cohort, who underwent medical and dental examinations in 1990 and were followed for five years. After five years, 52 of the 175 dentate subjects had died. Using univariate analysis, the association between baseline periodontitis and mortality was of borderline significance. After controlling for the common risk factors, periodontitis more than doubled the risk of cardiovascular disease-related mortality (HR 2.28, CI 1.03-5.05). The increase in total mortality was, however, not statistically significant (HR 1.43, CI 0.81-2.50). Subjects who were edentulous had higher mortality than those who were dentate without periodontitis, but the difference was not statistically significant. A baseline CRP level above 3 mg/l was associated with high mortality; but this effect was significant only among individuals with periodontitis. These results suggest that periodontitis influences the pathogenesis and outcome of cardiovascular disease, especially in individuals who also have evidence of a systemic inflammatory reaction.
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PMID:Periodontal disease and mortality in an aged population. 1476 90

During the last two decades, there has been an increasing interest in the impact of oral health on atherosclerosis and subsequent cardiovascular disease (CVD). The advent of the inflammation paradigm in coronary pathogenesis stimulated research in chronic infections caused by a variety of micro-organisms-such as Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus-as well as dental pathogens, since these chronic infections are thought to be involved in the etiopathogenesis of CVD by releasing cytokines and other pro-inflammatory mediators (e.g., C-reactive protein [CRP], tumor necrosis factor [TNF-alpha]) that may initiate a cascade of biochemical reactions and cause endothelial damage and facilitate cholesterol plaque attachment. Yet, due to the multi-factorial nature of dental infection and CVD, confirming a causal association is difficult, and the published results are conflicting. The main deficit in the majority of these studies has been the inadequate control of numerous confounding factors, leading to an overestimation and the imprecise measurement of the predictor or overadjustment of the confounding variables, resulting in underestimation of the risks. A meta-analysis of prospective and retrospective follow-up studies has shown that periodontal disease may increase the risk of CVD by approximately 20% (95% confidence interval [CI], 1.08-1.32). Similarly, the reported risk ratio between periodontal disease and stroke is even stronger, varying from 2.85 (CI 1.78-4.56) to 1.74 (CI 1.08-2.81). The association between peripheral vascular disease and oral health parameters has been explored in only two studies, and the resultant relative risks among individuals with periodontitis were 1.41 (CI 1.12-1.77) and 2.27 (CI 1.32-3.90), respectively. Overall, it appears that periodontal disease may indeed contribute to the pathogenesis of cardiovascular disease, although the statistical effect size is small.
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PMID:Oral health, atherosclerosis, and cardiovascular disease. 1557 81

Cardiovascular disease (CVD) and periodontitis are common chronic conditions, and the former remains a major contributor to human mortality. Recent attention has focused on a potential link between periodontal disease and CVD. Observational studies consistently indicate that people with destructive periodontitis may be 1.3 to 2 times more likely to have CVD. This association appears to be biologically plausible, and investigations in atherosclerosis animal models demonstrate larger atheroma sizes in animals infected with the periodontal pathogen, Porphyromonas gingivalis, compared with control animals. Although direct intervention data on the effects of periodontal therapy on CVD risk in patients are not currently available, indirect data suggest that mechanical periodontal therapy can decrease surrogate cardiovascular markers such as serum C-reactive protein. After a recent systematic review on the periodontal-cardiovascular link, a consensus panel concluded that patients and clinicians should be informed that periodontal therapy may prevent the onset or progression of CVD.
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PMID:The periodontal-cardiovascular link. 1564 98


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