Factors Associated with Dental Plaque, Gingivitis, and Caries in a Pediatric Population: A Records-Based Cross-Sectional Study

This retrospective, cross-sectional study evaluated dental records of 1000 healthy children to determine factors associated with plaque, gingivitis, and caries. A logistic model for plaque and gingivitis (mild versus moderate/severe) and caries (yes/no) was carried out separately for each variable using the following potential factors: Age, Gender, Brush Type, Starting Age of Brushing, Brushing Frequency, and Bite Type. Data from 998 children (median age: 4 years, 10 months (range: 2.5–7 years)) were analyzed. Sixty-four percent were manual toothbrush users; 36% were oscillating-rotating electric toothbrush users. For plaque and gingivitis, but not caries, Brush Type was more impactful than Brushing Frequency. Age influenced the severity of plaque and gingivitis, with increases in the odds of having moderate/severe plaque or gingivitis associated with increasing age. The probability of caries increased until approximately age 5 and then decreased until age 7. Oscillating-rotating brush users were more likely to present with less plaque, gingivitis, and caries, with 6.0, 5.1, and 1.4 times greater odds of having mild (versus moderate/severe) plaque, less severe gingivitis, and being caries-free, respectively, than manual brush users. Similarly, brushing twice daily and starting brushing at an earlier age were associated with better oral health outcomes. Children with anterior bite abnormalities had increased odds of developing moderate/severe plaque and gingivitis than children with normal anterior bites. Gender was not a statistically significant factor associated with plaque, gingivitis, or caries. Children’s oral health is influenced by toothbrush type, starting age of brushing, compliance with twice-daily brushing, and bite abnormalities

Dysregulation of the cohesin subunit RAD21 by Hepatitis C virus mediates host-virus interactions

Hepatitis C virus (HCV) infection is the leading cause of chronic hepatitis, which often results in liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCV possesses an RNA genome and its replication is confined to the cytoplasm. Yet, infection with HCV leads to global changes in gene expression, and chromosomal instability (CIN) in the host cell. The mechanisms by which the cytoplasmic virus affects these nuclear processes are elusive. Here, we show that HCV modulates the function of the Structural Maintenance of Chromosome (SMC) protein complex, cohesin, which tethers remote regions of chromatin. We demonstrate that infection of hepatoma cells with HCV leads to up regulation of the expression of the RAD21 cohesin subunit and changes cohesin residency on the chromatin. These changes regulate the expression of genes associated with virus-induced pathways. Furthermore, siRNA downregulation of viral-induced RAD21 reduces HCV infection. During mitosis, HCV infection induces hypercondensation of chromosomes and the appearance of multi-centrosomes. We provide evidence that the underlying mechanism involves the viral NS3/4 protease and the cohesin regulator, WAPL. Altogether, our results provide the first evidence that HCV induces changes in gene expression and chromosome structure of infected cells by modulating cohesin