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

Increasing evidence implicates periodontitis, a chronic inflammatory disease of the tooth-supporting structures, as a potential risk factor for increased morbidity or mortality for several systemic conditions including cardiovascular disease (atherosclerosis, heart attack, and stroke), pregnancy complications (spontaneous preterm birth [SPB]), and diabetes mellitus. Cross-sectional, case-control, and cohort studies indicate that periodontitis may confer two- and up to sevenfold increase in the risk for cardiovascular disease and premature birth, respectively. Given the recently acquired knowledge that systemic inflammation may contribute in the pathogenesis of atherosclerosis and may predispose to premature birth, research in the field of periodontics has focused on the potential of this chronic low-grade inflammatory condition to contribute to the generation of a systemic inflammatory phenotype. Consistent with this hypothesis clinical studies demonstrate that periodontitis patients have elevated markers of systemic inflammation, such as C-reactive protein (CRP), interleukin 6 (IL-6), haptoglobin, and fibrinogen. These are higher in periodontal patients with acute myocardial infarction (AMI) than in patients with AMI alone, supporting the notion that periodontal disease is an independent contributor to systemic inflammation. In the case of adverse pregnancy outcomes, studies on fetal cord blood from SBP babies indicate a strong in utero IgM antibody response specific to several oral periodontal pathogens, which induces an inflammatory response at the fetal-placental unit, leading to prematurity. The importance of periodontal infections to systemic health is further strengthened by pilot intervention trials indicating that periodontal therapy may improve surrogate cardiovascular outcomes, such as endothelial function, and may reduce four- to fivefold the incidence of premature birth. Nevertheless, further research is needed to fully discern the underlying mechanisms by which local chronic infections can have an impact on systemic health, and in this endeavor periodontal disease may serve as an ideal disease model.
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PMID:Low-grade inflammation in chronic infectious diseases: paradigm of periodontal infections. 1719 71

Severe marginal periodontitis often coexists with diabetes and is considered to be the sixth complication of the disease. Several factors associated with diabetes have been shown to be related to the development and deterioration of diabetic periodontitis, i.e., glycated hemoglobin (HbA(1C)), advanced glycation endproducts (AGEs), C-reactive protein (CRP), and glucose tolerance, as well as inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. A periodontal pathogen, Porphyromonas gingivalis with the type II fimbria gene, is also considered to be a related infectious factor. Among them, AGEs seem to be closely associated with the periodontitis deterioration seen in diabetic subjects. Osteoporosis and diabetes are also tightly related, and AGEs have been reported to accelerate the progression of osteoporosis. Collectively, AGEs are a critical diabetic factor to deteriorate oral osteoporosis.
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PMID:[Diabetes and oral osteoporosis]. 1727 75

Salivary secretions contain a variety of molecules that reflect important pathophysiological activities. Quantitative changes of specific salivary biomarkers could have significance in the diagnosis and management of both oral and systemic diseases. Modern point-of-care technologies with enhanced detection capabilities are needed to implement a significant advancement in salivary diagnostics. One such promising technology is the recently described lab-on-a-chip (LOC) assay system, in which assays are performed on chemically sensitized beads populated into etched silicon wafers with embedded fluid handling and optical detection capabilities. Using this LOC system, complex assays can be performed with small sample volumes, short analysis times, and markedly reduced reagent costs. This report describes the use of LOC methodologies to assess the levels of interleukin-1beta (IL-1beta), C-reactive protein (CRP), and matrix metalloproteinase-8 (MMP-8) in whole saliva, and the potential use of these biomarkers for diagnosing and categorizing the severity and extent of periodontitis. This study demonstrates that the results achieved by the LOC approach are in agreement with those acquired with standard enzyme-linked immunosorbent assay (ELISA), with significant IL-1beta and MMP-8 elevations in whole saliva of periodontitis patients. Furthermore, because of the superior detection capacities associated with the LOC approach, unlike those with ELISA, significant differences in CRP levels between periodontitis patients and normal subjects are observed. Finally, principal component analysis (PCA) is performed to yield an efficient method to discriminate between periodontally healthy and unhealthy patients, thus increasing the diagnostic value of these biomarkers for periodontitis when examined with the integrated LOC sensor system.
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PMID:Lab-on-a-chip methods for point-of-care measurements of salivary biomarkers of periodontitis. 1743 46

There is considerable debate over the relationship between periodontal and cardiovascular disease. It has been postulated that inflammatory mediators prevalent in periodontal disease may impact on atheroma formation and the thrombotic process. In cross-sectional, observational studies, periodontitis is associated with elevated C-reactive protein (CRP), hyperfibrinogenaemia and moderate leukocytosis. CRP levels have also been shown to decrease following periodontal therapy. CRP is a reliable marker of the acute phase reaction to infections and/or inflammation and is a powerful predictor of future coronary events.
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PMID:Change in cardiovascular risk status after dental clearance. 1772 53

This literature review summarizes current knowledge on the systemic levels of selected markers of inflammation in periodontitis. From the available literature it appears that the total numbers of leukocytes and plasma levels of C-reactive protein (CRP) are consistently higher in periodontitis patients compared with healthy controls. Some systemic markers of inflammation discussed in this review are also regarded as predictive markers for cardiovascular diseases. Therefore changes in these markers in periodontitis may be part of the explanation why periodontitis is associated with cardiovascular diseases and/or cerebrovascular events in epidemiological studies. It is hypothesized that possibly daily episodes of a bacteremia originating from the periodontal lesion are the cause of the changes in systemic markers in periodontitis; the overall size of periodontal lesions in the untreated severe patient may amount to 1500-2000 mm2.
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PMID:Systemic effects of periodontitis. 1766 87

The relationship between periodontitis and two measures of systemic inflammation, serum albumin and C-reactive protein (CRP), were examined among patients who were receiving chronic outpatient hemodialysis. Adult patients at two locations, North Carolina and New York City, were evaluated by dentist examiners. Six sites per tooth (up to 32 teeth per patient) were examined. A periodontitis case was defined as > or = 60% of sites with attachment level > or = 4 mm. Multivariable logistic regression was used to determine the association of periodontitis with low serum albumin, defined as < 3.5 mg/dl, and with high CRP, defined as > 3.0 mg/dl. A total of 154 patients completed the study. The mean age was 54.6 yr (SD 13.3), and average duration of dialysis was 4.0 yr (3 mo to 16 yr). Eighty-six (54.6%) were men, and 89 (58.2%) were black. Common causes of end-stage kidney disease were hypertension (12.3%), diabetes (22.1%), glomerulonephritis (7.1%), and other (58.4%). The average number of teeth was 20.3 (SD 8.4). Thirty-five (23%) patients were periodontitis cases. Severe periodontitis was associated with low serum albumin (odds ratio 8.20; 95% confidence interval 1.61 to 41.82; P = 0.01) compared with individuals without severe periodontitis disease after adjustment for age, gender, race, diabetes, hypertension, body mass index, smoking, study site, total cholesterol, serum calcium, serum phosphorus, and normalized protein catabolic rate. There was no observed association of severe periodontitis with CRP. Investigation of the potential contribution of periodontitis to serum albumin and possibly to morbidity and mortality among patients with end-stage kidney disease seems warranted.
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PMID:Severe periodontitis is associated with low serum albumin among patients on maintenance hemodialysis therapy. 1769 19

Periodontitis increases the atherosclerosis risk, but information on the role of periodontal pathogens in atherogenesis is limited. In the present study we have investigated, whether the major periodontal pathogen, Aggregatibacter (Actinobacillus) actinomycetemcomitans, induces development of atherosclerosis in apolipoprotein E-deficient mice. The mice received 4, 6, or 8 weekly i.v. injections of live pathogen (10(7)CFU/50 microl/mouse) or saline as control, and were killed 1 week after the last injection. The atherosclerotic lesion formation was examined from whole aortas and aortic sinus cryosections after lipid staining. Neither the lesion area in the aortas or en face analyses, nor their immunoreactivity to the macrophage-marker CD68 differed significantly between the infected and the control mice. However, the pathogen administration increased serum C-reactive protein (CRP) concentrations, and induced proatherogenic lipoprotein profiles with smaller particle sizes in very-low density (VLDL), low density (LDL), and high density (HDL) lipoprotein fractions. It also caused elevated matrix metalloproteinase-9 expression in the aortas and increased serum gelatinase level. Lipopolysaccharide deriving from the pathogen was associated with proatherogenic lipoprotein fractions: VLDL and especially LDL. The results indicate that A. actinomycetemcomitans contributes to disturbed lipoprotein profiles, inflammatory reaction, and matrix remodelling which are known to promote the development of atherosclerosis.
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PMID:Aggregatibacter actinomycetemcomitans induces MMP-9 expression and proatherogenic lipoprotein profile in apoE-deficient mice. 1788 99

Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.
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PMID:Oral infection, hyperglycemia, and endothelial dysfunction. 1790 6

Resolvin E1 (RvE1) is a potent proresolving mediator of inflammation derived from omega-3 eicosapentaenoic acid that acts locally to stop leukocyte recruitment and promote resolution. RvE1 displays potent counter-regulatory and tissue-protective actions in vitro and in vivo. Periodontal disease is a local inflammatory disease initiated by bacteria characterized by neutrophil-mediated tissue injury followed by development of a chronic immune lesion. In this study, we report the treatment of established periodontitis using RvE1 as a monotherapy in rabbits compared with structurally related lipids PGE(2) and leukotriene B(4). PGE(2) and leukotriene B(4) each enhanced development of periodontitis and worsened the severity of disease. Promotion of resolution of inflammation as a therapeutic target with RvE1 resulted in complete restoration of the local lesion, and reduction in the systemic inflammatory markers C-reactive protein and IL-1beta. This report is the first to show that resolution of inflammation by a naturally occurring endogenous lipid mediator results in complete regeneration of pathologically lost tissues, including bone.
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PMID:Resolvin E1 regulates inflammation at the cellular and tissue level and restores tissue homeostasis in vivo. 1798 93

The purpose of this study was to evaluate endothelial function in patients with periodontitis. We evaluated forearm blood flow responses to acetylcholine and sodium nitroprusside in patients with periodontitis who had no other cardiovascular risk factors (32 men; 25+/-3 years of age), in a normal control group (20 men; 26+/-3 years of age), and in hypertensive patients with periodontitis (28 men and 10 women; 56+/-12 years of age) and without periodontitis (control group; 18 men and 6 women; 54+/-13 years of age). Forearm blood flow was measured using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the control group. Both in healthy and hypertensive subjects, forearm blood flow responses to acetylcholine were significantly smaller in the periodontitis group than in the control group. Sodium nitroprusside-stimulated vasodilation was similar in the 2 groups. Periodontal therapy reduced serum concentrations of C-reactive protein and interleukin-6 and augmented acetylcholine-induced vasodilation in periodontitis patients with and without hypertension. After administration of N(G)-monomethyl-L-arginine, an NO synthase inhibitor, forearm blood flow response to acetylcholine was similar before and after treatment. These findings suggest that periodontitis is associated with endothelial dysfunction in subjects without cardiovascular risk factors, as well as hypertensive patients, through a decrease in NO bioavailability and that systemic inflammation may be, at least in part, a cause of endothelial dysfunction, leading to cardiovascular diseases.
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PMID:Periodontal infection is associated with endothelial dysfunction in healthy subjects and hypertensive patients. 1803 79


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