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A study was conducted to test the hypothesis that high consumption of soft drinks, relative to milk and 100% fruit juice, is a risk factor for dental caries in low-income African-American children in Detroit. Findings show that children who changed from being low consumers of soft drinks at baseline to high consumers after two years had a 1.75 times higher mean number of new decayed, missing, and filled tooth surfaces.

A study on the relationship between consumption of nonmilk extrinsic sugars and intrinsic milk sugars, and formation of dental caries in young children aged between 4.5 to 6.9 years of age, is presented.

Purpose: To assess the role of sociodemographic, dietary, and clinical factors in early mutans streptococci (MS) colonization in children aged 6 to 24 months who were followed for 18 months.Materials and Methods: Ninety-four children (mean age: 11.5 ± 4.99 months at baseline) were enrolled in the study from the Women, Infants and Children Supplemental Nutrition Program during 2003-2004. Salivary MS levels of the children were determined at baseline and at 18 months using a semi-quantitative method. Detailed information about the children's beverage consumption pattern, dietary behavior, and clinical information about oral health status was collected at baseline, 9 months, and 18 months. None of the children included in this study had detectable levels of MS at baseline.Results: Of the 94 children at baseline, 36 (38%) had acquired MS by the 18-month follow-up. The presence of >5 teeth [OR = 3.55 (1.46-9.04); p = 0.0062] was a significant risk factor for MS acquisition among the baseline variables. At 9 months, sports drinks consumption [OR = 5.56 (1.39-26.26); p = 0.0143] and presence of caries [OR = 9.36 (2.55-40.90); p < 0.0001] were significantly associated with MS colonization at 18 months. Higher maternal education [OR = 0.3 (0.07-1.36); p = 0.0351] was a protective factor at all the time points.Conclusion: Sugared beverage consumption, tooth-related factors, and lower maternal education can predict MS acquisition in young children. [ABSTRACT FROM AUTHOR]

Byline: Marcia C. Willing (1,6), James C. Torner (2), Trudy L. Burns (3), Kathleen F. Janz (4), Teresa Marshall (5), Julie Gilmore (5), Sachi P. Deschenes (1,5), John J. Warren (5), Steven M. Levy (5) Keywords: Bone; Bone mineral density; Children; COL1A2; Genetic polymorphisms; Osteocalcin Abstract: We examined the association of candidate gene polymorphisms with bone mineral density (BMD) and bone mineral content (BMC) in a cohort of 428 healthy non-Hispanic white children participating in the Iowa Bone Development Study, a longitudinal study of determinants of bone accrual in childhood. BMD and BMC measurements of the hip, spine and whole body were made using a Hologic 2000 Plus densitometer in 228 girls and 200 boys ages 4.5--6.5 years. Genotypes at 14 loci representing eight candidate genes [type I collagen genes (COL1A1 and COL1A2), osteocalcin, osteonectin, osteopontin, vitamin D receptor (VDR), estrogen receptor (ER), androgen receptor (AR)] were determined. Gender-specific and gender-combined prediction models for bone measures that included age, weight, height (and gender) were developed using multiple linear regression analysis. COL1A2 and osteocalcin genotypes were identified as having the strongest and most consistent association with BMD/BMC measures. Osteonectin, osteopontin and VDR translation initiation site polymorphisms were associated with some individual bone measures, but none of the associations was as consistent as those identified for the COL1A2 and osteocalcin genes. No association was identified with COL1A1 (RsaI and Sp1), VDR (BsmI) and ER polymorphisms (PvuII, XbaI, TA) and BMD/BMC. However, we identified significant gene-by-gene interaction effects involving the ER and both VDR and osteocalcin, which were associated with BMD/BMC. Our data suggest that genetic variation at multiple genetic loci is important in bone accrual in children. Moreover, the combination of genotypes as several loci may be as important as a single genotype for determining BMD and BMC. Author Affiliation: (1) Department of Pediatrics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA, 52242, USA (2) Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, IA, 52242, USA (3) Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, IA, 52242, USA (4) Department of Health, Leisure and Sports Studies, College of Liberal Arts, University of Iowa, Iowa City, IA, 52242, USA (5) Department of Preventive and Community Dentistry, College of Dentistry, University of Iowa, Iowa City, IA, 52242, USA (6) Department of Pediatrics, 2609 JCP, Division of Medical Genetics, University of Iowa, Iowa City, IA, 52242, USA Article History: Received Date: 02/09/2002 Accepted Date: 20/03/2003 Online Date: 22/07/2003