BackgroundMost studies have investigated the association between parental socioeconomic factors and dental caries in children based on educational and income levels; studies focusing on parental occupation, however, have been relatively limited. This cross-sectional study examined the associations between parental occupations and levels of education and household income and the prevalence of dental caries in Japanese children aged 3 years.MethodsStudy subjects were 6315 children. Oral examination results were obtained from the parents or guardians, who transcribed the information recorded by medical staff at a public health center from their maternal and child health handbooks to our self-administered questionnaire. Children were classified as having dental caries if one or more primary teeth had decayed or had been filled. Adjustment was made for sex, age, region of residence, breastfeeding duration, between-meal snack frequency, toothbrushing frequency, use of fluoride, regular dental check-ups, maternal smoking during pregnancy, and living with at least one household smoker.ResultsThe prevalence of dental caries was 14.7%. Compared with having an unemployed father, having a father employed in professional and engineering, clerical, sales, security, or manufacturing process was significantly associated with a lower prevalence of dental caries. Compared with having an unemployed mother, having a mother employed in professional and engineering or service was significantly inversely associated with the prevalence of dental caries. Significant inverse associations were observed between parental levels of education and household income and the prevalence of dental caries.ConclusionsThe findings of our study suggest that parental occupation affects the prevalence of dental caries in children. We confirm that higher levels of parental education and household income decreased the prevalence of dental caries.

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The Raman microprobe technique was applied for analysis of the molecular components at the adhesive interface between 4-META/MMA-TBB resin and dentin. The Raman spectra showed that the 4-META molecules in monomer solution were mostly hydrolyzed into 4-MET molecules, which were then co-polymerized with MMA molecules to form resin and resin-reinforced dentin layers. On the basis of line analysis by the Raman microprobe, resin molecules were estimated to penetrate 6 microns into the dentin from the interface. Raman intensity studies indicated that the concentration of 4-MET molecular units in the resin-reinforced dentin was more than four times the concentration in the original monomer solution. This demonstrated the excellent infiltration ability of 4-MET monomer into dentin substrate in situ.

Munksgaard EC, Hansen EK, Kato H: Wall-to-wall polymerization contraction of composite resins versus filler content. Scand J Dent Res 1987; 95: 52^31.Abstract -Various amounts of microiiller, condensed microfiller, prepoiymer plus microliller, or macrofilier were added to an unfilled light-curable resin. The marginal adaptation of these experimental resin/liller mixtures was studied by measuring the wall-to-wall polymerization contraction (wtw-eontraetion) in dentin eavities in vitro. The investigation showed that increasing amounts of microfiiler did not affect the wtw-eontraction. However, mixtures made by the three other fillers showed a decreasing wtw-eontraction with increasing filler concentration.

Background Sarcopenia with chronic kidney disease (CKD) progression is associated with life prognosis. Oxidative stress has attracted interest as a trigger for causing CKD‐related muscular atrophy. Advanced oxidation protein products (AOPPs), a uraemic toxin, are known to increase oxidative stress. However, the role of AOPPs on CKD‐induced muscle atrophy remains unclear. Methods In a retrospective case–control clinical study, we evaluated the relationship between serum AOPPs levels and muscle strength in haemodialysis patients with sarcopenia (n = 26, mean age ± SEM: 78.5 ± 1.4 years for male patients; n = 22, mean age ± SEM: 79.1 ± 1.5 for female patients), pre‐sarcopenia (n = 12, mean age ± SEM: 73.8 ± 2.0 years for male patients; n = 4, mean age ± SEM: 74.3 ± 4.1 for female patients) or without sarcopenia (n = 12, mean age ± SEM: 71.3 ± 1.6 years for male patients; n = 7, mean age ± SEM: 77.7 ± 1.6 for female ). The molecular mechanism responsible for the AOPPs‐induced muscle atrophy was investigated by using 5/6‐nephrectomized CKD mice, AOPPs‐overloaded mice, and C2C12 mouse myoblast cells. Results The haemodialysis patients with sarcopenia showed higher serum AOPPs levels as compared with the patients without sarcopenia. The serum AOPPs levels showed a negative correlation with grip strength (P < 0.01 for male patients, P < 0.01 for female patients) and skeletal muscle index (P < 0.01 for male patients). Serum AOPPs levels showed a positive correlation with cysteinylated albumin (Cys‐albumin), a marker of oxidative stress (r2 = 0.398, P < 0.01). In the gastrocnemius of CKD mice, muscle AOPPs levels were also increased, and it showed a positive correlation with atrogin‐1 (r2 = 0.538, P < 0.01) and myostatin expression (r2 = 0.421, P < 0.05), but a negative correlation with PGC‐1α expression (r2 = 0.405, P < 0.05). Using C2C12 cells, AOPPs increased atrogin‐1 and myostatin expression through the production of reactive oxygen species via CD36/NADPH oxidase pathway, and decreased myotube formation. AOPPs also induced mitochondrial dysfunction. In the AOPPs‐overloaded mice showed that decreasing running time and hanging time accompanied by increasing AOPPs levels and decreasing cross‐sectional area in gastrocnemius. Conclusions Advanced oxidation protein products contribute to CKD‐induced sarcopenia, suggesting that AOPPs or its downstream signalling pathway could be a therapeutic target for the treatment of CKD‐induced sarcopenia. Serum AOPPs or Cys‐albumin levels could be a new diagnostic marker for sarcopenia in CKD.