Oral Health Literacy in Migrant and Ethnic Minority Populations: A Systematic Review.

Cultural background influences how migrants and ethnic minority populations view and assess health. Poor oral health literacy (OHL) may be a hindrance in achieving good oral health. This systematic review summarizes the current quantitative evidence regarding OHL of migrants and ethnic minority populations. The PubMed database was searched for original quantitative studies that explore OHL as a holistic multidimensional construct or at least one of its subdimensions in migrants and ethnic minority populations. 34 publications were selected. Only 2 studies specifically addressed OHL in migrant populations. Generally, participants without migration background had higher OHL than migrant and ethnic minority populations. The latter showed lower dental service utilization, negative oral health beliefs, negative oral health behavior, and low levels of oral health knowledge. Due to its potential influence on OHL, oral health promoting behavior, attitudes, capabilities, and beliefs as well as the cultural and ethnic background of persons should be considered in medical education and oral health prevention programs.

Genetic Susceptibility Contributing to Periodontal and Cardiovascular Disease.

Periodontal disease (PD) and coronary artery disease (CAD) are common diseases characterized by an overaggressive inflammatory response to diverse stimuli. Whereas PD leads to destruction of the tooth-supporting structures, CAD is a chronic inflammatory condition ultimately causing myocardial infarction via narrowing and occluding of blood vessels. Classical twin studies led to the conclusion that both complex diseases have a similar degree of heritability and that a significant fraction of the genetic factors accounting for this heritability is shared. Recent genome-wide association and large-scale candidate gene studies highlight that variations in >50 genes are associated with premature CAD, while variations in only 4 genes showing nominally significant associations with aggressive periodontitis and/or chronic periodontitis have so far been identified. Remarkably, 3 of the PD loci (75%) show shared associations with CAD ( ANRIL/CDKN2B-AS1, PLG, CAMTA1/VAMP3), suggesting involvement of common pathogenic mechanisms. In this critical review, we highlight recent progress in identifying genetic markers and variants associated with PD, present their overlap with CAD, and discuss functional aspects. In addition, we answer why a significant fraction of the heritability of PD is still missing, and we suggest approaches that may be taken to close the gap.

Impact of lipoprotein(a) levels and apolipoprotein(a) isoform size on risk of coronary heart disease.

OBJECTIVES: Observational and genetic studies have shown that lipoprotein(a) [Lp(a)] levels and apolipoprotein(a) [apo(a)] isoform size are both associated with coronary heart disease (CHD) risk, but the relative independence of these risk factors remains unclear. Clarification of this uncertainty is relevant to the potential of future Lp(a)-lowering therapies for the prevention of CHD. METHODS: Plasma Lp(a) levels and apo(a) isoform size, estimated by the number of kringle IV (KIV) repeats, were measured in 995 patients with CHD and 998 control subjects. The associations between CHD risk and fifths of Lp(a) levels were assessed before and after adjustment for KIV repeats and, conversely, the associations between CHD risk and fifths of KIV repeats were assessed before and after adjustment for Lp(a) levels. RESULTS: Individuals in the top fifth of Lp(a) levels had more than a twofold higher risk of CHD compared with those in the bottom fifth, and this association was materially unaltered after adjustment for KIV repeats [odds ratio (OR) 2.05, 95% confidence interval (CI) 1.38-3.04, P < 0.001]. Furthermore, almost all of the excess risk was restricted to the two-fifths of the population with the highest Lp(a) levels. Individuals in the bottom fifth of KIV repeats had about a twofold higher risk of CHD compared with those in the top fifth, but this association was no longer significant after adjustment for Lp(a) levels (OR 1.13, 95% CI 0.77-1.66, P = 0.94). CONCLUSIONS: The effect of KIV repeats on CHD risk is mediated through their impact on Lp(a) levels, suggesting that absolute levels of Lp(a), rather than apo(a) isoform size, are the main determinant of CHD risk.

Heterozygosity for lysosomal acid lipase E8SJM mutation and serum lipid concentrations.

BACKGROUND AND AIM: The complete absence of the lysosomal acid lipase (LAL) enzyme function causes Wolman's Disease that is fatal within the first six months of life. Subtotal defects cause Cholesteryl ester storage disease (CESD), an autosomal recessive disorder leading to hepatic steatosis, fibrosis, micronodular cirrhosis, combined hyperlipidemia with low HDL-cholesterol, increased risk for atherosclerosis, premature death. Since the frequency of the Exon 8 splice junction mutation (c.894 G > A, E8SJM), the CESD leading mutation, is not rare in the general population (allele frequency 0.0025), we investigated the impact of this mutation on serum lipid profile in E8SJM carriers. METHODS AND RESULTS: We collected E8SJM carriers both form genetic study-population analysis and from Outpatient Lipid Clinics and then we assessed their serum lipid profile. We found thirteen individuals heterozygote for E8SJM. Most of them were Germans, three Spanish and two Italian. We found a significant increase in total cholesterol levels in both sexes with E8SJM mutation, leading to a significant increase in LDL cholesterol in males. CONCLUSIONS: Our results show that LAL E8SJM carriers have an alteration in lipid profile with a Polygenic Hypercholesterolemia phenotype, leading to an increase in cardiovascular risk profile.

Cardiovascular risk assessment in the metabolic syndrome: results from the Prospective Cardiovascular Munster (PROCAM) Study.

OBJECTIVES: We aimed (1) to construct a modified PROCAM risk algorithm, which incorporates BMI/waist circumference in a model for predicting coronary events; (2) to evaluate how accurate this and the previously established PROCAM risk algorithm predict coronary risk in individuals with metabolic syndrome. DESIGN: Prospective Cardiovascular Münster (PROCAM) Study, a prospective study of men and women at work in the northwest of Germany. SUBJECTS: A total of 7134 men aged 35-65 years at study entry. MEASUREMENTS: On the basis of 404 major coronary events (defined as nonfatal MI and coronary deaths), which occurred within 10 years of follow-up, a modified PROCAM risk algorithm was constructed by incorporating BMI/waist circumference as fixed variable in a Cox proportional hazards model for predicting coronary events. The metabolic syndrome was defined according to the latest recommendations proposed by the NCEP-ATP III Panel. RESULTS: Men who were classified as having the metabolic syndrome (n=2325, prevalence: 32.6%) were 2.59-fold more likely to experience a major coronary event within 10 years of follow-up than men not having the metabolic syndrome. In men with metabolic syndrome, the observed major coronary event rate of 9.6% corresponded well with their estimated global risk according to the modified BMI-based PROCAM risk algorithm (10.2%). Comparative calculations performed with the previously published fully adjusted PROCAM algorithm yielded very similar results. CONCLUSION: Both PROCAM algorithms provide very accurate means to ascertain coronary risk in male patients with metabolic syndrome.

Assessing risk of myocardial infarction and stroke: new data from the Prospective Cardiovascular Münster (PROCAM) study.

OBJECTIVES: Based on the data of the Prospective Cardiovascular Münster (PROCAM) study, a prospective study of men and women at work in the north-west of Germany, we aimed (i) to develop a refined scoring scheme for calculating the risk of acute coronary events among adult and elderly men and women; and (ii) to generate a new scoring scheme for calculating the risk of ischaemic stroke or transient ischaemic attack (TIA). METHODS: The coronary risk score was derived from a Weibull function using data from 18 460 men and 8515 women who were recruited before 1996 and had a mean follow-up period of 12+/-6 years. The stroke score was derived using a Cox proportional hazards model using data of 5905 men and 2225 women aged 35-65 years with at least 10 years of unbroken follow-up. RESULTS: The coronary risk score was based on 511 major coronary events, 462 (168 fatal, 294 non-fatal) in men and 49 (18 fatal, 31 non-fatal) in women and included the risk factors LDL cholesterol, HDL cholesterol, systolic blood pressure, smoking status, triglycerides and diabetes mellitus status. It was accurate in both sexes over an age range from 20 to 75 years with an area under the receiver-operating characteristics (ROC) curve of 0.82. The stroke score was based on 85 cerebral ischaemic events (21 TIAs, 64 ischaemic strokes) and included the risk factors age, sex, diabetes mellitus status, smoking status and systolic blood pressure. It had an area under the ROC curve of 0.78 and identified a high-risk group comprising only 4% of the study population that contained 31% of all cerebral ischaemic events. CONCLUSION: Both new PROCAM risk scores provide simple and effective ways to assess the risk of acute coronary events and ischaemic stroke in the general population and will improve the ability of physicians to target measures in an effort to prevent these potentially devastating conditions.

A mutation in the enamelin gene in a mouse model.

Amelogenesis imperfecta is an inherited disorder affecting tooth enamel formation. We previously isolated a mouse strain with an amelogenesis imperfecta phenotype (ATE1 mice) from a dominant ethylnitrosourea screen and mapped the disease-causing defect to a 9-cM region of mouse chromosome 5. In the current study, we tested the hypothesis that there is a mutation in enamelin (ENAM) or ameloblastin (AMBN), both of which are located within the linkage region, by sequencing these two candidate genes. Analysis of our data shows that the amelogenesis imperfecta phenotype is linked to a C > T transition in exon 8 of the enamelin gene. The mutation predicts a C826T transition, which is present in the enamelin transcript and changes the glutamine (Gln) codon at position 176 into a premature stop codon (Gln176X). Conversely, no mutation could be detected in the ameloblastin gene. These results define the ATE1 mice as a model for local hypoplastic autosomal-dominant amelogenesis imperfecta (AIH2), which is caused by enamelin truncation mutations in humans.

Association of peroxisome proliferator-activated receptor delta +294T/C with body mass index and interaction with peroxisome proliferator-activated receptor alpha L162V.

OBJECTIVE: To investigate the association of a polymorphism at position 294 (+294T/C) in the Peroxisome Proliferator-activated Receptor delta (PPARdelta) with body mass index (BMI) and the additional role of a gene-to-gene interaction between PPARdelta, PPARalpha and PPARgamma. DESIGN: An association between genetic variations in PPARdelta, PPARalpha and PPARgamma and indices of obesity and metabolism. SUBJECTS: A group of 462 moderately obese (mean BMI 28.9+/-7.7) and dyslipidemic, middle-aged (mean age 43.9+/-13.7), Caucasion men and women. MEASUREMENTS: The three most frequent single-nucleotide-polymorphisms (snp) in PPARdelta (+294T/C), PPARalpha (L162V) and PPARgamma (P12A) were genotyped and associated with clinical parameters. RESULTS: The C allele in PPARdelta was significantly associated with a lower body mass index. Moreover an interaction between the polymorphisms in PPARalpha and PPARdelta on body weight could be demonstrated. CONCLUSION: Our data provide further evidence for an involvement of PPARdelta in the regulation of BMI.

Polymorphisms in the apolipoprotein A5 (APOA5) gene and type III hyperlipidemia.

The great majority of patients with type III hyperlipidemia (type III HLP) are homozygous for the epsilon2 allele of the APOE gene. However, only about 10% of epsilon2 homozygotes develop type III HLP, and it has been proposed that additional genetic factors are required for the development of the condition. The frequency of two polymorphisms in the APOA5 gene, -1131T>C and S19W, has been determined in 72 hyperlipidemic patients with APOE2/2 genotype attending a lipid clinic. The frequency of both polymorphisms was significantly higher in APOE2/2 patients than in the normal population. Fifty-three percent of APOE2/2 patients were carriers of one of the polymorphisms compared to 19.7% of controls. Thus, genetic variation in the APOA5 gene is an important cofactor in the development of type III HLP.