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Objectives: The objectives of this cross-sectional survey were to determine the prevalence of secondary caries (SC) in general population, to identify patient- and material-related factors which may affect the prevalence, and to describe some clinical characteristics of SC lesions. Materials and methods: A total of 4036 restorations in 450 patients, who visited the university dental clinic for a regular (half) yearly checkup, were examined clinically (and radiographically) for the presence of SC. Clinical characteristics of the detected SC lesions (size, activity, and location) and the planned treatment were recorded. In addition, patients' caries-risk status was assessed according to the modified "cariogram" model. Results: In total, 146 restorations were diagnosed with SC, which gives an overall prevalence of 3.6%. Restorative material, restoration class, patient's caries risk, and smoking habits were shown to be important factors, as SC prevalence was significantly higher with composites, class II restorations, high-caries-risk patients, and smokers. Restorations' gingival margins were most frequently affected by SC. The largest number of restorations with SC (72%) was scheduled for the replacement. Conclusions: Prevalence of SC was higher with composite than with amalgam restorations, irrespective of the patient's caries-risk status. Gingival margins of class II, including MOD restorations, seem to be the place of less resistance to SC development. Management of SC seems to place a considerable burden on the health care workforce and expenditure. Clinical relevance: Secondary caries (SC) is considered to be the main cause of dental restoration failure and one of the biggest clinical challenges related to dental composites. Nevertheless, its prevalence in daily practice is still not clear, which impedes an accurate estimation of its impact on health care costs. [ABSTRACT FROM AUTHOR]

Background: In spite of contradicting results, the high susceptibility of composites for secondary caries is still often associated with the bacterial growth-stimulating effect of released methacrylate monomers. However, most studies that showed this effect were performed with techniques having inherent limitations (spectrophotometry). Objectives: Therefore, our objective was to determine the effect of four methacrylate monomers (2-Hydroxyethyl methacrylate (HEMA), triethylene glycol dimethacrylate (TEGDMA), ethylene glycol dimethacrylate (EGDMA), diethylene glycol dimethacrylate (DEGDMA)) on the growth of two caries-associated bacteria, Streptococcus mutans and sobrinus, and one non-cariogenic species, Streptococcus sanguinis, using TaqMan quantitative polymerase chain reaction (qPCR) to quantify bacterial DNA. Materials and methods: Cultures were exposed to monomer solutions selected after spectrophotometric growth measurements. At baseline and predetermined time intervals, bacterial DNA was extracted and quantified with TaqMan qPCR. Biofilms grown in the presence of monomers were analyzed with scanning electron microscopy (SEM). Results: Spectrophotometry indeed showed increased growth rates of all three strains with 5 mM TEGDMA, EGDMA, and DEGDMA and increased total biomass of S. sanguinis with 5 mM TEGDMA. However, qPCR failed to show any growth-stimulating effect of these monomers on S. mutans and S. sobrinus. In contrast, some monomers exhibited a growth-inhibiting effect on S. sanguinis. SEM revealed extracellular matter in S. sobrinus and S. sanguinis biofilms, which might be attributed to polymer formation. Conclusions: Techniques which quantify bacterial DNA are more appropriate to evaluate bacterial growth in the presence of monomers than spectrophotometry. Clinical relevance: Even though methacrylate monomers did not affect the growth of cariogenic species, growth inhibition of S. sanguinis, a non-cariogenic antagonistic species, may lead to ecological shifts towards higher cariogenicity. [ABSTRACT FROM AUTHOR]

Coronary microcirculatory function after primary percutaneous coronary intervention (pPCI) in patients with acute myocardial infarction is important determinant of infarct size (IS). Our aim was to investigate the utility of coronary flow reserve (CFR) and diastolic deceleration time (DDT) of the infarct artery (IRA) assessed by transthoracic Doppler echocardiography after pPCI for final IS prediction. In 59 patients, on the 2nd day after pPCI for acute anterior myocardial infarction, transthoracic Doppler analysis of IRA blood flow was done including measurements of CFR, baseline DDT and DDT during adenosine infusion (DDT adeno). Killip class, myocardial blush grade, resolution of ST segment elevation, peak creatine kinase-myocardial band and conventional echocardiographic parameters were determined. Single-photon emission computed tomography myocardial perfusion imaging was done 6 weeks later to define final IS (percentage of myocardium with fixed perfusion abnormality). IS significantly correlated with CFR (r = −0.686, p < 0.01), DDT (r = −0.727, p < 0.01), and DDT adeno (r = −0.780, p < 0.01). CFR and DDT adeno in multivariate analysis remained independent IS predictors after adjustment for other covariates and offered incremental prognostic value in models based on conventional clinical, angiographic, electrocardiographic and enzymatic variables. In predicting large infarction (IS > 20 %), the best cut-off for CFR was <1.73 (sensitivity 65 %, specificity 96 %) and for DDT adeno ≤720 ms (sensitivity 81 %, specificity 96 %). CFR and DDT during adenosine are independent and powerful early predictors of final IS offering incremental prognostic information over conventional parameters of myocardial and microvascular damage and tissue reperfusion. [ABSTRACT FROM AUTHOR]

Copyright of Herz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Herz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Despite existing reports on differential DNA methylation in type 2 diabetes (T2D) and obesity, our understanding of its functional relevance remains limited. Here we show the effect of differential methylation in the early phases of T2D pathology by a blood-based epigenome-wide association study of 4808 non-diabetic Europeans in the discovery phase and 11,750 individuals in the replication. We identify CpGs in LETM1, RBM20, IRS2, MAN2A2 and the 1q25.3 region associated with fasting insulin, and in FCRL6, SLAMF1, APOBEC3H and the 15q26.1 region with fasting glucose. In silico cross-omics analyses highlight the role of differential methylation in the crosstalk between the adaptive immune system and glucose homeostasis. The differential methylation explains at least 16.9% of the association between obesity and insulin. Our study sheds light on the biological interactions between genetic variants driving differential methylation and gene expression in the early pathogenesis of T2D. Our understanding of the functional link between differential DNA methylation and type 2 diabetes and obesity remains limited. Here the authors present a blood-based EWAS of fasting glucose and insulin among 4808 non-diabetic Europeans and identify nine CpGs not previously implicated in glucose, insulin homeostasis and diabetes. [ABSTRACT FROM AUTHOR]