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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral conditions such as gingivitis and chronic periodontitis are found worldwide and are among the most prevalent microbial diseases of mankind. The cause of these common inflammatory conditions is the complex microbiota found as dental plaque, a complex microbial biofilm. Despite 3000 years of history demonstrating the influence of oral status on general health, it is only in recent decades that the association between periodontal diseases and systemic conditions such as coronary heart disease and stroke, and a higher risk of preterm low birth-weight babies, has been realised. Similarly, recognition of the threats posed by periodontal diseases to individuals with chronic diseases such as diabetes, respiratory diseases and osteoporosis is relatively recent. Despite these epidemiological associations, the mechanisms for the various relationships remain unknown. Nevertheless, a number of hypotheses have been postulated, including common susceptibility, systemic inflammation with increased circulating cytokines and mediators, direct infection and cross-reactivity or molecular mimicry between bacterial antigens and self-antigens. With respect to the latter, cross-reactive antibodies and T-cells between self heat-shock proteins (HSPs) and Porphyromonas gingivalis GroEL have been demonstrated in the peripheral blood of patients with atherosclerosis as well as in the atherosclerotic plaques themselves. In addition, P. gingivalis infection has been shown to enhance the development and progression of atherosclerosis in apoE-deficient mice. From these data, it is clear that oral infection may represent a significant risk-factor for systemic diseases, and hence the control of oral disease is essential in the prevention and management of these systemic conditions.
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PMID:Relationship between periodontal infections and systemic disease. 1771 90

Werner syndrome (WS) is a rare autosomal recessive genetic instability/cancer predisposition disorder that displays many symptoms of premature aging. The mimicry of agerelated phenotypes in WS, as well as its dependence on a single defective gene product, has provided the impetus for studying this fascinating disease as a model system for normative aging and its related pathologies such as atherosclerosis, neoplasia, diabetes mellitus, and osteoporosis. The gene product defective in WS, WRN, is a member of the RecQ DNA helicase family that is widely distributed in all kingdoms of life, and is believed to play a central role in genomic stability by preferentially operating on non-canonical DNA structures. Although there have been considerable advances in our understanding of the biochemistry of WRN and its interacting protein partners, the in vivo molecular function(s) of WRN remain(s) elusive. In addition to summarizing the features and clinical progression of WS, the following chapter details our current understanding of the WRN protein with respect to its biochemistry and its interacting protein partners, and considers its putative in vivo roles in various DNA transactions.
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PMID:Werner Syndrome, aging and cancer. 1872 62

The XXth century is marked by the substantial increase in human life expectancy. Historically, main reasons for that are four achievements of medicine: (1) improvements in common hygiene, such as waste disposal and water purification which led to the significant reduction of communicable diseases; (2) common recognition of Pasteur's Germ Theory followed by improvements in occupational and personal hygiene as well as introduction of antiseptic and aseptic measures; (3) decrease in childhood mortality due to the discovery and widespread application of vaccination; and (4) the discovery and clinical application of antibiotics. An epidemiological transition took place, i.e. the shift from communicable infectious diseases, as a main cause of morbidity and mortality, to chronic degenerative diseases, mainly considered non-infectious. Experimental evidence has been accumulated on a significant number of microorganisms, including viruses (such as a group of herpes viruses, hepatitis viruses, etc.), bacteria (Chlamydia, Helicobacter, periodontal pathogens, etc.), fungi and parasites, as an underlying reason for many of diseases, such as atherosclerosis, various cancers, type 1 and 2 diabetes, neurodegenerative and some psychiatric diseases, osteoporosis, autoimmune diseases and others. On the other hand, most of these diseases have been traditionally associated with age, together with other "age-related" disorders, such as immune system suppression, thymus involution, pathologic calcification, etc. Taken together, these facts suggest that aging, among others, has infectious origins, and that burden of infections may lead to enhanced senescence and premature death. In fact, infections may serve as a trigger of senescence, presumably via the mechanisms of chronic oxidative stress, low-grade inflammation, telomere shortening, and autoimmune processes due to the molecular mimicry. We believe that next step in human longevity increase can be possible by common appreciation of the role of infections as the main trigger of age-related diseases and disorders, and by efforts to cure and/or eradicate these infections.
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PMID:[Fifth revolution in medicine: on the role of infections in pathogenesis of aging and chronic diseases]. 1882 37

Environmental factors, especially viruses, are thought to play an important role in the initiation or acceleration of the pathogenesis of type 1 diabetes (T1D). Data from retrospective and prospective epidemiological studies strongly suggest that enteroviruses, such as coxsackievirus B4 (CV-B4), may be associated with the development of T1D. It has also been shown that enterovirus infections are significantly more prevalent in at-risk individuals such as the siblings of diabetic patients, when they develop anti-beta-cell autoantibodies or T1D, and in recently diagnosed diabetic patients, compared with control subjects. The isolation of CV-B4 from the pancreas of diabetic patients supports the hypothesis of a relationship between the virus and the disease. Furthermore, studies performed in vitro and in vivo in animal models have increased our knowledge of the role of CV-B4 in T1D by helping to clarify the pathogenic mechanisms of the infection that can lead to beta-cell destruction, including direct virus-induced beta-cell lysis, molecular mimicry, 'bystander activation' and viral persistence. The role of enteroviruses as the sole agents in T1D, and a causal link between these agents and T1D, have not yet been established, although arguments that support such a role for these viruses in the pathogenesis of the disease cannot be ignored.
Diabetes Metab 2008 Dec
PMID:Role of coxsackievirus B4 in the pathogenesis of type 1 diabetes. 1895 21

The hypervariable (Vbeta/D/Jbeta) regions of T-cell receptors (TCR) have been sequenced in a variety of autoimmune diseases by various investigators. An analysis of some of these sequences shows that TCR from both human diabetics and NOD mice mimic insulin, glucagon, the insulin receptor, and the glucagon receptor. Such similarities are not found in the TCR produced in other human autoimmune diseases. These data may explain how insulin, glucagon, and their receptors are targets of autoimmunity in diabetes and also suggest that TCR mimicking insulin and its receptor may be targets of anti-insulin autoantibodies. Such intra-systemic mimicry of self-proteins also raises complex questions about how "self" and "nonself" are regulated during TCR production, especially in light of the complementarity of insulin for its receptor and glucagon for its receptor. The data presented here suggest that some TCR may be complementary to other TCR in autoimmune diseases, a possibility that is experimentally testable. Such complementarity, if it exists, could either serve to down-regulate the clones bearing such TCR or, alternatively, trigger an intra-immune system civil war between them.
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PMID:Autoreactive T-cell receptor (Vbeta/D/Jbeta) sequences in diabetes are homologous to insulin, glucagon, the insulin receptor, and the glucagon receptor. 1905 Dec 6

A role for the ubiquitous Torque teno (TT) viruses in the pathogenesis of disease has not been resolved. In vivo and in vitro intragenomic rearrangement of TT virus genomes has been demonstrated. Replication in cell culture of a subviral molecule (411 bp) occurs through oligomerisation of RNA transcripts. Although the functions of the respective TT viral genes, as well as the newly formed genes in the rearranged subviral molecules, are largely unknown, certain similarities to genes of plant viruses of the family Geminiviridae will be described. A degree of similarity to certain cellular genes poses the question as to a role of molecular mimicry in the pathogenesis of autoimmune disease and diabetes.
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PMID:Intragenomic rearrangement in TT viruses: a possible role in the pathogenesis of disease. 1923 May 59

Infection by various viral and bacterial pathogens has long been proposed as one of the etiologies of autoimmune diabetes. Many theories, ranging from direct cytolysis of pancreatic islet cells to immunological processes such as antigen mimicry and polyclonal lymphocyte activation, tried to explain the epidemiological correlation between infections and diabetes, supported by information from human and animal studies. However, a direct correlation and exact mechanism continue to elude investigators due to scarce and conflicting data. Interestingly, there is also data to support an opposite role for infection in the development of type 1 diabetes, as several pathogens demonstrated a protective effect from this disease. This article reviews the current data available from clinical studies and animal models, while trying to explain the different mechanisms underlying these findings.
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PMID:Infection and type 1 diabetes mellitus - a two edged sword? 1939 95

Diabetes mellitus is accompanied by hormonal and neurochemical changes that can be associated with anxiety and depression. Both diabetes and depression negatively interact, in that depression leads to poor metabolic control and hyperglycemia exacerbates depression. We hypothesize one novel vanadium complex of vanadium-enriched Cordyceps sinensis (VECS), which is beneficial in preventing depression in diabetes, and influences the long-term course of glycemic control. Vanadium compounds have the ability to imitate the action of insulin, and this mimicry may have further favorable effects on the level of treatment satisfaction and mood. C. sinensis has an antidepressant-like activity, and attenuates the diabetes-induced increase in blood glucose concentrations. We suggest that the VECS may be a potential strategy for contemporary treatment of depression and diabetes through the co-effect of C. sinensis and vanadium. The validity of the hypothesis can most simply be tested by examining blood glucose levels, and swimming and climbing behavior in streptozotocin-induced hyperglycemic rats.
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PMID:A Contemporary Treatment Approach to Both Diabetes and Depression by Cordyceps sinensis, Rich in Vanadium. 1994 51

Immunopathologic reactions may occur during toxocariasis due to tissue invasion and destruction by the secretions of larvae containing various enzymes with broad spectrum. The aim of this study was to search for autoantibodies such as anti-nuclear (ANA), anti-mitochondrial (AMA), anti-smooth muscle (ASMA), anti-neutrophil cytoplasmic (ANCA), anti-myeloperoxidase (MPO) and liver-kidney microsomal type 1 (LKM-1) antibodies in patients with toxocariasis, in order to investigate the role of toxocariasis as a trigger factor for autoimmune reactions. Forty patients (22 were male; mean age: 35.6 +/- 10.7 years) diagnosed as toxocariasis by clinical findings (abdominal pain, allergic symptoms and/or eosinophilia, without detection of any other causative agents, and without liver dysfunction, diabetes mellitus, cardiac or renal failure, and autoimmune disease) and in-house ELISA positivity and 32 healthy controls (16 were male; mean age: 40.7 +/- 11.2 years) were included to the study. ANA (screen), dsDNA, SS-A, SS-B, Scl-70, LKM-1, MPO and M2 autoantibodies have been investigated by ELISA (Euroimmun, Germany), while ANCA, AMA and ASMA antibodies by indirect immunofluorescence (IMMCO, NY) methods. Autoantibody positivity was detected in 18 (45%) patients of whom 11 yielded a single type, and 7 yielded > or = 2 types of autoantibodies. This rate was 12.5% for control group (two subjects were positive for ANA-Screen, one for anti-M2 and one for anti-LKM-1). The difference between the total positivity rates in patient and control groups was found statistically significant (chi2 = 5.72, p = 0.004). The most frequent autoantibody type among patients were ASMA (n = 6), followed by anti-dsDNA (n = 5), anti-M2 (n = 5), anti-SS-B (n = 4), anti-LKM-1 (n = 3), anti-SS-A (n = 2), ANCA (n = 2) and anti-MPO (n = 1). Positivity rate for ASMA was found statistically significant in patients' group compared to controls (chi2 = 12.24, p = 0.03), while there was no significant difference between the groups in terms of other autoantibody rates (p> 0.05). These data could be related to the possible release of autoantigens following muscle tissue injury during toxocariasis and/or antigenic mimicry of parasitic products during the infection in which muscle invasion is frequently seen. In conclusion, since autoantibodies are frequently detected in toxocariasis, this situation should be taken into consideration in the presence of autoantibodies.
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PMID:[Investigation of the presence of autoantibodies in patients with toxocariasis]. 2008 21

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


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