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Dental caries is still a common disease among children and adolescents. The aims of the present thesis were therefore: 1) to investigate the approximal caries prevalence in posterior teeth in 15-year-olds, 2) to study past caries experience in the primary dentition in relation to future caries development and need for treatment, 3) to investigate factors during early childhood which are associated with caries development later in life, and 4) to study the association between age-specific body mass index (isoBMI) and approximal caries status in 15-year-olds. Paper I has a retrospective design and the analyses were based on record data from a randomly selected sample. Papers II, III and IV are based on radiographic analyses of posterior teeth in 15-year-olds followed longitudinally from 1 to 15 years of age. The data for these studies were selected from examinations, interviews and questionnaires from early childhood and school health care records at 15 years (isoBMI values). The result showed that the approximal caries prevalence in 15-year-olds is underestimated in official caries data, since initial caries lesions are not included in these statistics. Two thirds of all 15-year-olds had approximal caries and initial caries constituted 86% of the total number of caries lesions. There was a strong relationship between caries in early childhood and approximal caries prevalence in the posterior teeth at 15 years of age. Children with caries experience at 6 years received significantly more treatment in the primary dentition during the period from 7 to 12 years compared with children who were caries free at the same age. Further, it was pointed out that parents' attitudes to dental health and psychosocial factors during early childhood have an effect on approximal caries in 15-year-olds. Additionally, plaque on primary incisors at 1 year of age and infrequent toothbrushing at 3 years of age were associated with a high caries experience at 15 years. It was also demonstrated that adolescents with overweight and obesity had a significantly higher approximal caries prevalence than those of normal weight. Furthermore, it was shown that children's unfavourable snacking habits at 1 and 3 years of age were associated with approximal caries at 15 years. The main conclusions from this thesis are that: 1) epidemiologicalcaries data should include initial caries lesions on approximal tooth surfaces, in order to show the actual caries prevalence, 2) there is a strong relationship between caries in early childhood and approximal caries prevalence in the posterior teeth at 15 years of age, 3) the psychosocial environment in which children live during their childhood has an impact on dental health later in life, 4) good oral hygiene habits including the use of fluoride toothpaste, established in early childhood, provide a foundation for good dental health in adolescence, and 5) future preventive programmes should include, at a multidisciplinary level, strategies to prevent and reduce both dental caries and obesity at an early age.
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PMID:On dental caries and caries-related factors in children and teenagers. 1863 15

The mortality rate after myocardial infarction fell sharply with the advent of reperfusion methods and the use of efficient antithrombotic and antiischemic drugs. However, new infarcts, heart failure, arrythmias and sudden death remain frequent, especially in the first two years after the initial event. Large clinical studies have defined and validated therapies for secondary prevention, but the recommended measures are not always properly implemented. Patients with and without ST elevation after myocardial infarction share the same pathophysiologic mechanism, namely atherosclerotic plaque rupture or erosion, with different degrees of superimposed thrombosis and distal embolization. Secondary prevention is the same for these two patient categories. Acute coronary syndromes are associated with an increased risk of adverse cardiovascular outcomes (new myocardial ischemia, left ventricular dysfunction or sudden death) and require aggressive secondary prevention. However, risks factors such as smoking, hypertension, obesity, hypercholesterolemia and diabetes frequently persist. In addition, medical practice does not always respect consensus guidelines. Early risk stratification is necessary to detect residual myocardial ischemia in viable myocardium. After the acute phase, the prognosis depends on the degree of left ventricular dysfunction and the extent and severity of residual ischemia. Exercise and ambulatory electrocardiography, stress echocardiography, perfusion scintigraphy using vasodilator stress, magnetic resonance imaging and coronary angiography are all useful for identifying high-risk patients. Secondary prevention should include risk factor management with lifestyle modifications such as weight reduction, a reduction in saturated fats and an increase in monounsaturated fatty acids. Smoking cessation is crucial, and regular physical activity (30 min per day at least 5 days a week) is beneficial. Cardiac rehabilitation has been shown to improve exercise tolerance and cardiovascular outcome.
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PMID:[Secondary prevention after myocardial infarction]. 1866 72

The metabolic syndrome is a common and complex disorder combining obesity, dyslipidemia, hypertension, and insulin resistance. It is a primary risk factor for diabetes and cardiovascular disease. We showed for the first time that the metabolic syndrome is associated with a higher fraction of oxidized LDL and thus with higher levels of circulating oxidized LDL. Hyperinsulinemia and impaired glycaemic control, independent of lipid levels, were associated with increased in vivo LDL oxidation, as reflected by the higher prevalence of high oxidized LDL. High levels of oxidized LDL were associated with increased risk of future myocardial infarction, even after adjustment for LDL-cholesterol and other established cardiovascular risk factors. This association is in agreement with the finding that accumulation of oxidized LDL, which activates/induces subsets of smooth muscle cells and macrophages to gelatinase production, was associated with upstream localization of a vulnerable plaque phenotype. Dyslipidemia and insulin resistance in obese LDL receptor-deficient mice were associated with increased oxidative stress and impaired HDL-associated antioxidant defence associated with accelerated atherosclerosis due to increased macrophage infiltration and accumulation of oxidized LDL in the aorta. The accumulation of oxidized LDL was partly due to an impaired HDL-associated antioxidant defence due to a decrease in PON. Our data in this experimental model are thus the more relevant because a decrease in PON activity was found to be associated with a defective metabolism of oxidized phospholipids by HDL from patients with type 2 diabetes. Weight loss in leptin-deficient, obese, and insulin-resistant mice was associated with expressional changes of key genes regulating adipocyte differentiation, glucose transport and insulin sensitivity, lipid metabolism, oxidative stress and inflammation, most of which are under the transcriptional control of PPARs. We established an important relationship between PPAR-gamma and SOD1 for the prevention of the oxidation of LDL in the arterial wall. For example we showed that rosuvastatin decreased the oxidized LDL accumulation by increasing the expression of PPAR-gamma and SOD1. In addition, we established a relation between increased PPAR-alpha expression in the adipose tissue and a change in the gene expression pattern, which explains the decrease of free fatty acids, triglycerides and the increase in insulin sensitivity. We demonstrated that plaque oxidized LDL correlated with coronary plaque complexity in a swine atherosclerosis model. Oxidized LDL correlated positively with the expression of IRF1 and TLR2 suggesting a relation between oxidative stress and inflammation in coronary atherosclerotic plaques. Oxidized LDL induced further the expression of TLR2 and IRF1 in macrophages in vitro suggesting a causative link. As in the mouse model described above, plaque oxidized LDL correlated negatively with SOD1 expression and ox-LDL inhibited the expression of SOD1 in macrophages in vitro. We showed that TLR2, CXCR4 and MYC are overexpressed in monocytes of obese women at high cardiovascular risk and that weight loss was associated with a concomitant decrease of their expression. This suggests that the transcription factor cMYC has an atherogenic effect by inducing pro-inflammatory genes. The increased expression of TLR2 and CXCR4 were observed in the absence of an increase in ox-LDL but in the presence of an increase in SOD1. Interestingly, the expression of SOD1 correlated also with that of MYC, suggesting that it has an atherogenic effect by inducing the expression of an anti-oxidant enzyme. How ox-LDL prevents this increase remains to be determined. How we plan to do this is explained in the next part. In aggregate, our studies contributed to a better understanding of the relationships between metabolic syndrome, insulin signalling, oxidative stress and inflammation and atherosclerosis. We identified paraoxonase, interferon regulatory factor-1, toll-like receptors, CXCR4 and SOD1 as possible targets for intervention.
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PMID:Relations between metabolic syndrome, oxidative stress and inflammation and cardiovascular disease. 1866 60

Shortly after the introduction of oral contraceptives in 1960, myocardial infarction (MI) started to emerge as a major adverse effect. Its mechanism and pathophysiology have remained elusive. Many epidemiological studies identified smoking, hypertension, diabetes and hypercholesterolemia as risk factors for coronary thrombosis in young women using oral contraceptives. The pathogenesis of MI involves two phases: atherosclerotic plaque formation, and thrombotic arterial occlusion. The use of very low doses of estrogen (less than 50 microg of ethinyl estradiol) and new progestagens have minimized the vascular risks. However, the risk remains in women who smoke or have other atherosclerotic risks factors. We report 12 cases of MI in women aged 35 +/- 5 years who were using different types of oral contraceptive. All the women had several risks factors, such as smoking, hypertension, hypercholesterolemia, obesity, and type II diabetes. Coronarography during the acute phase showed either occlusions on severe atherosclerotic stenoses or thrombosis of arteries with non significant atherosclerotic plaque. In two cases coronarography was normal after thrombolysis. Ten women recovered without sequelae, but reversible left ventricular dysfunction occurred in the other two women, who did not have acute-phase revascularization. Recent case-control studies show that the cardiovascular risk is very low with new, third-generation combined contraceptives. But the risk of MI increases with age, smoking, hypertension, dyslipidemia and diabetes. The absolute risks associated with oral contraceptives and smoking are higher in women over 35, because of the steeply rising incidence of atherosclerosis. It is mandatory to respect the classical contraindications of oral contraception.
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PMID:[Myocardial infarction and oral contraceptives]. 1881 1

Coronary heart disease (CHD) remains the leading cause of death in the United States. Immune mechanisms have been recently proposed to play an important role in the development of atherosclerotic plaques in CHD. Heat shock proteins and oxidized low-density lipoprotein are proinflammatory substances that have been shown to have an important role in the pathogenesis of atherosclerosis, and are now targets for clinical vaccine development. In addition, a vaccine has been developed to inhibit cholesteryl ester transfer protein. It is now recognized that many medications used to combat plaque development and rupture have significant anti-inflammatory effects and these effects are critical for drug efficacy. The influenza vaccine is associated with an atheroprotective effect. In addition, a nicotine vaccine, an antiangiotensin vaccine, and an anti-obesity vaccine may play a therapeutic role in modifying known risk factors for the development of atherosclerosis and its complications. This article reviews these vaccines as possible additions to the armamentarium of atheroprotective treatment modalities.
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PMID:Vaccines in development to prevent and treat atherosclerotic disease. 1892 32

The metabolic syndrome is a combination of diabetes mellitus type 2, hypertension, central obesity and combined hyperlipidemia. The metabolic syndrome and its components have been largely associated with psoriasis. We report the case of a 66-year-old man affected with metabolic syndrome and psoriasis in which a multidisciplinary approach with endocrinologists and nutritionists led to an improvement of both conditions. After only 4 months of diet and an appropriate therapeutic regimen we observed an improvement of the hyperglycaemia, dyslipidemia, significant lose of weight, BMI switching from obesity to overweight and improvement of plaque psoriasis in absence of other treatments. We report this case to emphasise the need of a major control of the metabolic syndrome and associated comorbidities in psoriatic patients. Moreover we suggest that diet counselling and regular nutritional visits should be recommended in some patients to obtain dual benefits.
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PMID:Does metabolic syndrome influence psoriasis? 1902 21

This study was designed to determine whether lipocalin type-prostaglandin D synthase (l-pgds) deficiency contributes to atherogenesis using gene knockout (KO) mice. A high-fat diet was given to 8-week-old C57BL/6 (wild type; WT), l-pgds KO (LKO), apolipoprotein E (apo E) KO (AKO) and l-pgds/apo E double KO (DKO) mice. The l-pgds deficient mice showed significantly increased body weight, which was accompanied by increased size of subcutaneous and visceral fat tissues. Fat deposition in the aortic wall induced by the high-fat diet was significantly increased in LKO mice compared with WT mice, although there was no significant difference between AKO and DKO mice. In LKO mice, atherosclerotic plaque in the aortic root was also increased and, furthermore, macrophage cellularity and the expression of pro-inflammatory cytokines such as interleukin-1beta and monocyte chemoattractant protein-1 were significant increased. In conclusion, l-pgds deficiency induces obesity and facilitates atherosclerosis, probably through the regulation of inflammatory responses.
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PMID:Knockout of the l-pgds gene aggravates obesity and atherosclerosis in mice. 1907 May 93

Atherosclerosis develops over the course of 50 years, beginning in the early teenage years. The causes of this process appear to be lipid retention, oxidation, and modification, which provoke chronic inflammation at susceptible sites in the walls of all major conduit arteries. Initial fatty streaks evolve into fibrous plaques, some of which develop into forms that are vulnerable to rupture, causing thrombosis or stenosis. Erosion of the surfaces of some plaques and rupture of a plaque's calcific nodule into the artery lumen also may trigger thrombosis. The process of plaque development is the same regardless of race/ethnicity, sex, or geographic location, apparently worldwide. However, the rate of development is faster in patients with risk factors such as hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predisposition. Clinical trial data demonstrate that treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) favorably alters plaque size, cellular composition, chemical composition, and biological activities centered on inflammation and cholesterol metabolism, as well as the risk of clinical events due to atherosclerosis. Even with advanced atherosclerosis, statins begin to improve clinical risk within 4 months. During long-term follow-up in clinical trials for up to 11 years with or without further treatment, clinical benefit remains significant, indicating the durability of treatment-induced changes in the development of plaque. Thus, atherosclerosis, a disease heretofore viewed as inevitably progressive, can be treated to significantly alter arterial lesions and reduce their clinical consequences.
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PMID:The pathology of atherosclerosis: plaque development and plaque responses to medical treatment. 1911 86

Patients with a coronary artery calcification score (CACS) of zero and an intermediate risk of coronary artery disease have been shown to have a low prevalence of non-calcified coronary artery plaque (NCP). 181 consecutive patients with CAC 'zero', undergoing cardiac computed tomography angiography (CCTA) angiography at our center were evaluated. Presence of detectable NCP on CCTA in these patients was 13.8%. Mild non-obstructive disease (<30% and limited to one segment) was present in 76% of patients while only one patient (0.6%) had significant stenosis (>50%). Traditional risk factors were not found to be associated with the presence of NCP. However higher body mass index (BMI) was strongly found to be associated with NCP (31.6 in patients with NCP vs. 27.6 kg/m(2) in patients without NCP, p<.05). Obesity was 2.76 times more likely to be associated with NCP as compared to normal BMI (p<0.05).
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PMID:Effect of obesity on coronary artery plaque using 64 slice multidetector cardiac computed tomography angiography. 1911 25

A relationship between psoriasis, pro-inflammatory cytokines and obesity has been demonstrated. Tumour necrosis factor-alpha (TNF-alpha), that is involved in the pathogenesis of psoriasis, is commonly over-expressed in obese subjects, and seems to be derived from inflammatory cells and adipocytes. The primary aim of this study is to investigate whether the Body Mass Index (BMI) of patients influences the clinical response to etanercept, a competitive inhibitor of TNF-alpha approved for the treatment of moderate-to-severe plaque-type psoriasis. The secondary aim is to evaluate whether the TNF-alpha inhibition influences the weight and BMI profile of patients. One hundred patients received 50 mg etanercept twice weekly for 12 weeks, followed by 25 mg. At weeks-12 and 24, treatment efficacy and tolerability were evaluated, as well as body weight and BMI. BMI values did not correlate with etanercept efficacy. Mean PASI score variation did not show significant differences among the BMI groups. A statistically significant weight gain and BMI variation were observed in a consistent rate of patients. Patient BMI does not influence psoriasis efficacy parameters. Although the role of anti TNF-alpha molecules on weight regulation need to be confirmed, our study shows that etanercept treatment may induce weight gain and a BMI increase.
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PMID:Influence and variation of the body mass index in patients treated with etanercept for plaque-type psoriasis. 1930 69


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