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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The overall objective with the present investigations was to study the influence of insulin-dependent diabetes mellitus (IDDM) on periodontal conditions and to identify factors that may be predictors for severe periodontal disease in individuals with IDDM. Periodontal conditions were studied in two cross-sectional studies of adult, insulin-dependent diabetics and age-and sex-matched controls. In one study 72 diabetics with short-(SD) and 82 with long-duration (LD) diabetes and 77 controls participated. In the other study 83 LD diabetics and 99 controls took part. The portion of individuals exhibiting severe periodontal disease was larger in the diabetic group than in the control group. Advanced periodontal disease appeared in earlier ages (40-49 years) in the LD diabetics compared to the SD diabetics and controls. In fact, the 40-49-year-old LD diabetics had alveolar bone loss equal to the older controls (60-69 years). LD diabetics exhibited more severe periodontitis than SD diabetics. Some salivary factors were studied in 72 SD and 82 LD diabetics and 77 controls. LD and SD diabetics had a lower stimulated salivary secretion rate and an increased glucose content compared to the controls. The reduction in flow rate, however, was moderate, and all mean values were within the normal limits. The moderately increased glucose content did not result in higher mean numbers of Candida albicans, lactobacilli, and mutans streptococci. The subgingival bacterial species currently considered to be associated with periodontitis were studied in 30 LD diabetics and 34 controls. All these bacterial species were recovered in diabetics as well as controls. More LD diabetics than controls harboured Porphyromonas gingivalis. In the control group the periopathogens were recovered more often in deep periodontal pockets. In the LD group, however, these bacterial species were recovered as often in shallow as in deep periodontal pockets. The medical status of 39 matched pairs of LD diabetics was analysed. One in each pair had severe periodontal disease while the other had no/minor symptoms of periodontal disease. Biochemical analyses and clinical variables routinely used in monitoring diabetics failed to discriminate between diabetics with severe and minor periodontal disease. Diabetics with severe periodontal disease, however, showed a higher prevalence of renal disease and cardiovascular complications such as stroke, transient ischemic attacks, angina, myocardial infarct, heart failure, and claudicatio intermittens than diabetics with only minor periodontal disease. This indicates that closer cooperation between the diabetologist and the dentist is necessary in monitoring the diabetic patient.
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PMID:Periodontal disease in adult insulin-dependent diabetics. 763 66

The aim of this study was to define a population of diabetics exhibiting an increased risk of developing severe periodontitis by comparing the medical status of 2 groups of diabetics, 1 with no/minor periodontal disease and 1 with severe periodontal disease. The case-control study consisted of 2 parts, a baseline study and a follow-up study. 39 case-control pairs were selected. They were adult, long-duration, insulin-dependent diabetics matched according to sex, age and diabetes duration. One individual in each pair (the CASE) exhibited severe periodontal disease while the other (the CONTROL) exhibited gingivitis or only minor alveolar bone loss. The median age of the cases was 58 years (range 36 to 70 years) and of the controls 59 years (range 37 to 69 years). The median disease duration in cases and controls was 24 years and 25 years, respectively. The median follow-up time was 6 years. The medical variables analysed were weight, insulin dose, systolic and diastolic blood pressure, vibratory threshold, triglycerides, total-cholesterol, HDL-cholesterol, creatinine, HbA1, proteinuria, ECG, retinopathy, stroke, transient ischemic attacks (TIA), angina, myocardial infarct, heart failure, hypertension, intermittent claudication, foot ulcer, death, cause of death, and smoking habit. Biochemical analyses and clinical variables used as a routine in the monitoring of diabetics failed to differentiate between diabetics with severe and minor periodontal disease. In the follow-up study, significantly higher prevalences of proteinuria and cardiovascular complications such as stroke, TIA, angina, myocardial infarct and intermittent claudication were found in the case group. An association between renal disease, cardiovascular complications and severe periodontitis seems to exist. This indicates that a closer cooperation between the diabetologist and the dentist is necessary in monitoring the diabetic patient.
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PMID:Medical status and complications in relation to periodontal disease experience in insulin-dependent diabetics. 870 78

Recent studies have shown that acute infections, especially of the respiratory tract, are an important risk factor for cerebral ischemia. Additionally we know that chronic dental infections may be a risk for myocardial infarction and artherosclerosis. However, the connection between stroke and dental infections has hardly been examined so far. Therefore we performed a case-control study using a standardized questionaire and examination. We investigated 66 patients consecutive to a acute cerebral ischemia/stroke and 60 age- and sex-matched nonstroke neurological patients as a control group. Dental status was determined by a so called total dental index (TDI) which reflects primarily caries, periodontitis, periapical lesions, devital and missing teeth as well as by a panoramic index (PI). Specifically, older patients with cerebrovascular ischemia tended to have a significantly worse dental status and had more severe periodontitis and periapical lesions than control subjects. A predefined poor dental status was associated with cerebrovascular ischemia independent from other vascular risk factors and social status. In conclusion, poor dental health, mainly resulting from chronic dental infections, may be associated with an increased risk for cerebrovascular ischemia. The results must now be verified in larger studies. As chronic dental infections are a common and also easily treatable factor, their identification as a risk factor for stroke would be quite important in the field of preventive medicine.
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PMID:[Odontogenic focus as the etiology of cerebral ischemia]. 988 Oct 1

In recent years substantial data accumulated in the literature supporting the direct detrimental effect of tobacco smoking on periodontal health. The significantly inferior periodontal condition of smokers cannot be solely attributed to poor oral hygiene, increased calculus formation and altered subgingival microflora. Smoking imposes a direct threat to the periodontal tissues. Smokers with excellent oral hygiene show significantly less periodontal bone height and attachment level than matches non-smokers. Smoking entails a 2.5 to 3.5 risk ratio for severe periodontal attachment loss. Smoking also interferes with the outcome of nonsurgical and surgical periodontal treatment and impairs periodontal regeneration. The pathomechanism of the tobacco smoking related periodontal destruction is just partly understood. Tobacco products can alter normal host responses to neutralize infections and can also stimulate pathologic mechanisms to destroy the surrounding tissues. Tobacco products can directly impair polymorphonuclear leukocyte functions. Smokers have less salivary IgA and decreased serum IgG concentration as well as depressed number of helper T lymphocytes. Consequently smoking today is considered as one of the major risk factors for destructive periodontitis. Periodontitis is also considered as a decisive risk factor for systemic diseases especially for cardiovascular disorders. A strong association has been shown between periodontal disease and coronary heart diseases, as well as between periodontal disease and cerebrovascular diseases (stroke). The subgingival microflora and the continuous latent bacteremia and endotoxemia originated from the periodontal pockets might be responsible for the damage of the vascular endothelial integrity, platelet functions and blood coagulation. Modern periodontal epidemiology rediscovered the old ide of "focal infections" and indicated that the general health has a crucial impact on the periodontal health and periodontal disease has also a major impact on the general health status of the patient.
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PMID:[The effect of smoking on the spread and frequency of periodontal disease]. 1033 78

The established risk factors for ischemic stroke do not sufficiently explain all clinical and epidemiological features of the disease, such as the winter peak of stroke incidence, the decline of stroke during this century and the time point of cerebral ischemia. A role of infectious disease as stroke risk factor may partly explain above features. Several case-control studies with both hospital and population control groups showed that acute infection within the preceding week and mainly respiratory infection of both viral and bacterial origin increase the risk of cerebral ischemia independent from other risk factors (odds ratio 2.9-14.5). Infection as a risk factor appears to be most important in young age groups. Infection may cause a procoagulant state and thus, trigger thrombosis and cerebral ischemia. There is increasing evidence for chronic infection as stroke risk factor. A case-control study indicated chronic and recurrent bronchitis to increase stroke risk. Two case-control and one cohort study showed that chronic dental infection, mainly parodontitis, is a risk factor for stroke. There are conflicting results on chronic infection with cytomegalovirus and insufficient evidence for a role of Helicobacter pylorii infection in pathogenesis of stroke. Seroepidemiological studies and analyses of carotid plaques indicate a role of Chlamydia pneumoniae in ischemic stroke. However, causality can not yet be inferred from present results. Acute and chronic infectious diseases are treatable and partly preventable conditions. Their recognition as stroke risk factors could therefore be important for stroke prevention.
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PMID:[Infection, atherosclerosis and acute ischemic cerebrovascular disease]. 1069 60

Cardiovascular disease is the leading cause of death in developed countries. The cause is multifactorial. A substantial proportion of patients with coronary artery disease (CAD) do not have traditional risk factors. Infectious diseases may play a role in these cases, or they may intensify the effect of other risk factors. The association of CAD and Chlamydia pneumoniae infection is firmly established, but causality is yet to be proven. The link with other infectious agents or conditions, such as cytomegalovirus, herpes simplex virus, Helicobacter pylori and periodontitis, is more controversial. Cytomegalovirus infection is more strongly linked than native CAD to coronary artery restenosis after angioplasty and to accelerated CAD after cardiac transplantation. However, new data on this topic are appearing in the literature almost every month. The potential for novel therapeutic management of cardiovascular disease and stroke is great if infection is proven to cause or accelerate CAD or atherosclerosis. However, physicians should not "jump the gun" and start using antibiotic therapy prematurely for CAD. The results of large randomized clinical trials in progress will help establish causality and the benefits of antimicrobial therapy in CAD.
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PMID:Emerging relations between infectious diseases and coronary artery disease and atherosclerosis. 1092 Jul 32

Periodontitis, a prime cause of tooth loss in humans, is implicated in the increased risk of systemic diseases such as heart failure, stroke, and bacterial pneumonia. The mechanisms by which periodontitis and antibacterial immunity lead to alveolar bone and tooth loss are poorly understood. To study the human immune response to specific periodontal infections, we transplanted human peripheral blood lymphocytes (HuPBLs) from periodontitis patients into NOD/SCID mice. Oral challenge of HuPBL-NOD/SCID mice with Actinobacillus actinomycetemcomitans, a well-known Gram-negative anaerobic microorganism that causes human periodontitis, activates human CD4(+) T cells in the periodontium and triggers local alveolar bone destruction. Human CD4(+) T cells, but not CD8(+) T cells or B cells, are identified as essential mediators of alveolar bone destruction. Stimulation of CD4(+) T cells by A. actinomycetemcomitans induces production of osteoprotegerin ligand (OPG-L), a key modulator of osteoclastogenesis and osteoclast activation. In vivo inhibition of OPG-L function with the decoy receptor OPG diminishes alveolar bone destruction and reduces the number of periodontal osteoclasts after microbial challenge. These data imply that the molecular explanation for alveolar bone destruction observed in periodontal infections is mediated by microorganism-triggered induction of OPG-L expression on CD4(+) T cells and the consequent activation of osteoclasts. Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis.
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PMID:Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection. 1099 85

In the past decade there has been renewed interest in the old hypothesis that infections increase the risk of developing cardiovascular disease and stroke. There is now a convincing body of evidence that atherosclerosis has a major inflammatory component and is much more than the simple vascular accumulation of lipids. Infectious agents that have been linked to an increased risk of coronary heart disease (CHD) include Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses. The concept has emerged that each of these agents is an independent risk factor for CHD and that common chronic infections are important. In addition, periodontal infections have also been implicated as one of several factors contributing to the development of CHD. Evidence supporting a causative role of chronic infections in CHD is largely circumstantial. However, the evidence is sufficiently strong to warrant further examination of the possible link between chronic infections and CHD. In this review the lines of evidence for a causative role of C. pneumoniae in the development of CHD are summarized and contrasted with the lines of evidence suggesting a periodontal infection--CHD association. If common or widespread chronic infections are truly important risk factors for CHD, it is unlikely that a single infection will be shown to be causative. It is likely that the entire microbial burden of the patient from several simultaneous chronic infections is more important (e.g., H. pylori-caused gastric ulcers + C. pneumoniae-caused bronchitis + periodontitis). Increased cooperation between cardiologists and periodontists will be required to determine if, and what, combinations of common chronic infections are important in the pathogenesis of CHD and stroke.
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PMID:Periodontal infections and cardiovascular disease--how strong is the association? 1135 66

The role of chronic infections in the initiation of atherosclerotic lesions has been vividly discussed in recent years. A possible causal relationship between cardiovascular diseases and infections with, e. g., Chlamydia pneumoniae, Helicobacter pylori, or herpes viruses had also been established for chronic periodontitis, in particular after discovery of DNA of typical periodontal pathogens in atheromatous plaques. Especially in longitudinal epidemiologic studies, a low or moderate association between existing periodontitis and the development of, e. g., coronary heart disease or non-haemorrhagic stroke had been observed. In this article the respective literature is critically reviewed. In particular, the influence of incomplete or inappropriate adjustment for common risk factors for both diseases, i. e., cardiovascular disease and periodontitis should be analysed. In metaanalyses of prospective studies, in which the respective endpoint occurred after the investigation had commenced, relative risks of periodontitis of 1.12 (95 % confidence interval 0.95-1.33) for coronary heart disease and 1.73 (0.89-3.34) for ischaemic stroke were calculated. Whether chronic periodontitis actually represents an important risk for the development of cardiovascular diseases remains questionable. Already planned intervention studies appear to be premature and ethically highly problematic.
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PMID:[Does chronic periodontitis play a role in the pathogenesis of cardiovascular and cerebrovascular diseases?]. 1190 48

Conventional periodontal therapy consists of mechanical scaling and root planing, and surgical treatment. This is still the mainstay of periodontal treatment. Adjunctive antimicrobial treatments, both systemic and local delivery, are becoming more sophisticated and useful in the treatment of recurrent periodontitis. Also very promising are adjunctive treatments that modulate the host response and decrease levels of destructive pro-inflammatory cytokines or matrix metalloproteinases. Smoking is a major risk factor for periodontitis and has a profound impact on the progression of periodontal bone and attachment loss. In the interest of improved periodontal health patients should be encouraged to stop smoking. Finally bacterial endotoxins that stimulate the release of pro-inflammatory cytokines can have systemic effects and may lead to pre-term, low birthweight babies, and cardiovascular diseases such as atherosclerosis, myocardial infarction and stroke. Health professionals need to be cognisant of the effect dental health can have on systemic diseases and refer for treatment when appropriate to ensure that optimum oral and systemic health is achieved for their patients.
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PMID:Emerging concepts in periodontal therapy. 1246 98


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