Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The detrimental effect of focal infection on general health has been known for decades. Chronic dental infections may worsen the condition of medically compromised patients. Prophylactic antibiotics are therefore routinely prescribed before dental treatment to immunosuppressed and other at-risk patients to combat the spread of oral bacteria into the bloodstream. More recent studies have shown that dental infections may also be a risk factor for atherosclerosis and various other chronic diseases, emphasizing the need for frequent dental checkups among the diseased, in particular. The aim of this review article is to discuss some recent findings on the effect of dental infections on health in general. In many industrialized countries, there is an urgent need to focus on preventive dental care for the diseased and the elderly, whose oral health has been more or less neglected.
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PMID:Dental infections and general health. 947 71

Although first suggested at the turn of the 20th century, there is a renewed interest in the infectious theory of atherosclerosis. Studies done in many laboratories around the world over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia, particularly in the early stages of reperfusion. It is also being recognized that the traditional risk factors, such as smoking, dyslipidemia, hypertension and diabetes mellitus, do not explain the presence of coronary atherosclerosis in a large proportion of patients. We believe that in certain genetically susceptible people, infection with very common organisms, such as Chlamydia pneumoniae or cytomegalovirus, may lead to a localized infection and a chronic inflammatory reaction. Persistence of infection may relate to the degree of inflammation and severity of atherosclerosis. Early trials with appropriate antibiotic agents in some patients with a recent history of acute myocardial infarction have led to very salutary results. If patients with an infectious basis of atherosclerosis can be identified, a therapy directed at eradication of the offending organism may be appropriate.
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PMID:Interactive role of infection, inflammation and traditional risk factors in atherosclerosis and coronary artery disease. 980 69

During past decades the relationship between dentistry and internal medicine and especially the concept of the so-called focal infection theory have long been a matter of debate. The pathogenesis of focal diseases has been classically attributed to dental pulp pathologies and periapical infections. Nonetheless, in recent years, their role is being dismissed while increasing interest is being devoted to the possible associations between periodontal infection and systemic diseases. In fact, periodontal pathogens and their products, as well as inflammatory mediators produced in periodontal tissues, might enter the bloodstream, causing systemic effects and/or contributing to systemic diseases. On the basis of this mechanism, chronic periodontitis has been suggested as a risk factor for cardiovascular diseases associated with atherosclerosis, bacterial endocarditis, diabetes mellitus, respiratory disease, preterm delivery, rheumatoid arthritis, and, recently, osteoporosis, pancreatic cancer, metabolic syndrome, renal diseases and neurodegenerative diseases such as Alzheimer's disease. Various hypotheses, including common susceptibility, systemic inflammation, direct bacterial infection and cross-reactivity, or molecular mimicry, between bacterial antigens and self-antigens, have been postulated to explain these relationships. In this scenario, the association of periodontal disease with systemic diseases has set the stage for introducing the concept of periodontal medicine. This narrative review summarizes the evolution of focal infection theory up to the current pathophysiology of periodontal disease, and presents an update on the relationships between chronic periodontitis and systemic diseases.
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PMID:Dentistry and internal medicine: from the focal infection theory to the periodontal medicine concept. 2157 Jun 29

There is increasing documentation of a link between inflammatory periodontal disease affecting the supporting structure of teeth, rheumatoid arthritis, and coronary artery disease. Periodontitis is initiated predominantly by Gram-negative bacteria and progresses as a consequence of the host inflammatory response to periodontal pathogens. Lipopolysaccharide, a cell wall constituent stimulates the production of inflammatory cytokines via the activation of signaling pathways perpetuating inflammatory pathogenesis in a cyclical manner in susceptible individuals; with an element of autoimmune stimulation, not dissimilar to the sequential events seen in RA. Periodontitis, also implicated as a risk factor for cardiovascular disease, promotes mechanisms for atherosclerosis by enhancing an imbalance in systemic inflammatory mediators; more direct mechanisms attributed to microbial products are also implicated in both RA and atherogenesis. Severe periodontal disease characterized by clinical and radiographic parameters has been associated with ischemic stroke risk, significant levels of C-reactive protein and serum amyloid A, amongst others common to both periodontitis and atherosclerosis. Existing data supports the hypothesis that persistent localized infection in periodontitis may influence systemic levels of inflammatory markers and pose a risk for RA and atherosclerosis. A common nucleus of activity in their pathogeneses provides novel paradigms of therapeutic targeting for reciprocal benefit.
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PMID:Association of periodontitis with rheumatoid arthritis and atherosclerosis: Novel paradigms in etiopathogeneses and management? 2778 92

Blood oxidative stress (BLOS) is the presence of white blood cells and platelets that are generating high levels of reactive oxygen species (ROS). A mathematical model links the level of BLOS or BLOS# and plasma sulfide concentration. An increase in the BLOS# reduces the plasma sulfide concentration. The reported maximum plasma sulfide concentration for defined health conditions were used to calculate the minimum BLOS#. Elevated BLOS generates high plasma concentration of ROS, which triggers multiple responses in the body that protect the host. First, insulin production by the pancreas is inhibited, which results in elevated blood glucose levels. This results in advanced glycation end products (AGE), which thicken the blood vessel wall. Elevated blood glucose levels also increases urination, which reduces the availability of substrates for infectious bacteria. Second, one or more signaling molecules are stimulated to produce vascular hypertrophy resulting in hypertension. Third, the initial stage of atherosclerosis thickens the blood vessel wall while also protecting the inner surface of the blood vessels from localized infection. The first three mechanisms provide added protection against pathogen migration through the blood vessel wall and reduce the cross-sectional area of blood vessels, which increases the retention time (RT) for improved ROS inactivation of pathogens. Fourth, genes expressed in the liver, which are associated with drug oxidation and uptake transport, are inhibited. This inhibition protects the host from any toxins produced by an anaerobic infection. Elevated BLOS also reduces plasma sulfide concentration, which inhibits wound healing and extends aerobic conditions of the wound. The normal induction of BLOS offers a short-term, cascade of several primary mechanisms for secondary defense against anaerobic infection of a wound. Normal induction of BLOS is due to ultra-exogenous sulfide formation (USF) generated by a local anaerobic infection of a wound in the natural environment. The presence of BLOS without infection is indicative of inadvertent dietary induction. Long-term dietary BLOS results in many severe inflammatory diseases and cancers that are common in an ageing population. Glands were identified as more susceptible to cancers caused by long-term dietary BLOS. Variable BLOS levels in patients of clinical trials may also be reducing effectiveness of experimental drugs and causing drug toxicity. If BLOS is confirmed as a secondary defense against infection that is inadvertently triggered by diet, then a large number of common health problems may be treated and managed by apheresis and dietary changes.
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PMID:Blood oxidative stress (BLOS) is a secondary host defense system responding normally to anaerobic wound infection and inadvertently to dietary ultra-exogenous sulfide formation (USF). 2801 99