573999
research-article2015
PENXXX10.1177/0148607115573999Journal of Parenteral and Enteral NutritionMerheb et al
Original Communication
Neonatal Serum Phosphorus Levels and Enamel Defects in Very-Low-Birth-Weight Infants Roula Merheb, MD1; Chitra Arumugam, MD2; Wonik Lee, PhD3; Marc Collin, MD1; Caroline Nguyen, MD1; Sharon Groh-Wargo, PhD, RD1; and Suchitra Nelson, PhD3
Journal of Parenteral and Enteral Nutrition Volume XX Number X Month 201X 1–7 © 2015 American Society for Parenteral and Enteral Nutrition DOI: 10.1177/0148607115573999 jpen.sagepub.com hosted at online.sagepub.com
Abstract Background: Very-low-birth-weight (VLBW) infants miss out on the period of greatest mineral accretion that occurs during the last trimester of pregnancy and are at higher risk of enamel defects. No studies have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. The objective of this study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects. Methods: A retrospective chart review of VLBW infants recruited for an ongoing longitudinal dental study between 2007 and 2010 was done. Participants were classified as cases and controls according to the presence/absence of developmental defects of enamel at 8 and/or 18–20 and/or 36 months. Demographics and medical and nutrition data were abstracted from 76 subjects’ medical charts. Results: Of the 76 VLBW subjects, 62% had enamel defects (hypoplasia and/or opacity). The only significant variable in the logistic regression analysis was that infants with a 1-mg/dL increase in serum phosphorus levels had a 68% reduction in the odds of having enamel hypoplasia (odds ratio, 0.322; P = .024). Conclusion: Neonatal lower serum phosphorus levels are significantly associated with enamel hypoplasia in VLBW infants younger than 3 years. (JPEN J Parenter Enteral Nutr. XXXX;xx:xx-xx)
Keywords very low birth weight; enamel defects; nutrition; calcium; phosphate; calcium homeostasis
Clinical Relevancy Statement Very-low-birth-weight (VLBW) infants miss out on the period of greatest mineral accretion that occurs during the last trimester of pregnancy and are at higher risk of enamel defects. No studies have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. The objective of this study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects.
Introduction Advances in medical technology and innovative nutrition practices in the neonatal period have resulted in improved survival of very-low-birth-weight (VLBW) infants. Approximately 1.5% of all live births are VLBW infants,1 and 72% survive to discharge.2 Major medical morbidities of these infants have remained static despite improved survival3 needing long-term health services.4 Most of the research has focused mainly on chronic morbidities such as neurodevelopmental outcomes, bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), and cognitive abilities.4 Dental health issues related to prematurity include enamel hypoplasia
of primary teeth, which can lead to increased susceptibility to early childhood caries (ECC).5 From the 1Department of Pediatrics, Division of Neonatology, MetroHealth Medical Center and Case Western Reserve University, Cleveland, Ohio, USA; 2Department of Pediatrics, Division of Neonatology, University of Louisville, Louisville, Kentucky, USA; and 3 Department of Community Dentistry, School of Dental Medicine, Case Western Reserve University, Cleveland, Ohio, USA. Financial disclosure: This study was supported by National Institutes of Health grant R01DE017947 from the National Institute of Dental and Craniofacial Research and by CTSC UL1RR024989 and CTSC UL1TR000439 from the National Center for Research Resources. Conflict of interest: The authors declare no conflict of interest. Supplementary material for this article is available on the Journal of Parenteral and Enteral Nutrition website at http://jpen.sagepub.com/ supplemental. Received for publication November 7, 2014; accepted for publication January 19, 2015. Corresponding Author: Roula Merheb, MD, Department of Pediatrics, Division of Neonatology, MetroHealth Medical Center and Case Western Reserve University, 2500 Metro Health Drive, Cleveland, OH, 44109, USA. Email: [email protected].
Downloaded from pen.sagepub.com at University of Otago Library on July 18, 2015
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Journal of Parenteral and Enteral Nutrition XX(X) mineralization of the enamel. Other comorbidities such as osteopenia, sepsis, patent ductus arteriosus (PDA), and intraventricular hemorrhage (IVH) during the neonatal period can negatively affect the absorption and metabolism of nutrients supply.20 To our knowledge, there are no studies that have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. We hypothesize that VLBW infants with enamel defects would have poorer nutrition status compared with VLBW infants without enamel defects. Thus, the objective of the study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects.
Figure 1. Enamel hypoplasia in the teeth of infants.
Subjects and Methods Enamel is a unique hard tissue in that it does not remodel. It is formed by mineralization of a protein matrix, which begins at about 14–15 weeks of gestation in utero and continues until late adolescence.6 Any insults during this period result in developmental defects of enamel (DDE), which consist of enamel hypoplasia and/or diffuse opacity and/or demarcated enamel.7 DDE is mainly caused by a dysregulation in calcium homeostasis resulting from systemic causes prenatally or postnatally and/or local causes such as endotracheal intubation in the postnatal period.8 Enamel hypoplasia is a common quantitative tooth defect in which there is a deficient amount of enamel, often resulting in discoloration and caries susceptibility9 (Figure 1). It is a biological marker for intrauterine stress, and in recent studies, it has been shown that individuals who had enamel hypoplasia in the neonatal period tend to be subject to earlier adolescent or adult mortality.10 Enamel opacity is another tooth defect that is defined as a qualitative change in the translucency of the enamel.11 Previous studies have described a higher prevalence of DDE in preterm patients with low birth weight (LBW;
research-article2015
PENXXX10.1177/0148607115573999Journal of Parenteral and Enteral NutritionMerheb et al
Original Communication
Neonatal Serum Phosphorus Levels and Enamel Defects in Very-Low-Birth-Weight Infants Roula Merheb, MD1; Chitra Arumugam, MD2; Wonik Lee, PhD3; Marc Collin, MD1; Caroline Nguyen, MD1; Sharon Groh-Wargo, PhD, RD1; and Suchitra Nelson, PhD3
Journal of Parenteral and Enteral Nutrition Volume XX Number X Month 201X 1–7 © 2015 American Society for Parenteral and Enteral Nutrition DOI: 10.1177/0148607115573999 jpen.sagepub.com hosted at online.sagepub.com
Abstract Background: Very-low-birth-weight (VLBW) infants miss out on the period of greatest mineral accretion that occurs during the last trimester of pregnancy and are at higher risk of enamel defects. No studies have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. The objective of this study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects. Methods: A retrospective chart review of VLBW infants recruited for an ongoing longitudinal dental study between 2007 and 2010 was done. Participants were classified as cases and controls according to the presence/absence of developmental defects of enamel at 8 and/or 18–20 and/or 36 months. Demographics and medical and nutrition data were abstracted from 76 subjects’ medical charts. Results: Of the 76 VLBW subjects, 62% had enamel defects (hypoplasia and/or opacity). The only significant variable in the logistic regression analysis was that infants with a 1-mg/dL increase in serum phosphorus levels had a 68% reduction in the odds of having enamel hypoplasia (odds ratio, 0.322; P = .024). Conclusion: Neonatal lower serum phosphorus levels are significantly associated with enamel hypoplasia in VLBW infants younger than 3 years. (JPEN J Parenter Enteral Nutr. XXXX;xx:xx-xx)
Keywords very low birth weight; enamel defects; nutrition; calcium; phosphate; calcium homeostasis
Clinical Relevancy Statement Very-low-birth-weight (VLBW) infants miss out on the period of greatest mineral accretion that occurs during the last trimester of pregnancy and are at higher risk of enamel defects. No studies have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. The objective of this study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects.
Introduction Advances in medical technology and innovative nutrition practices in the neonatal period have resulted in improved survival of very-low-birth-weight (VLBW) infants. Approximately 1.5% of all live births are VLBW infants,1 and 72% survive to discharge.2 Major medical morbidities of these infants have remained static despite improved survival3 needing long-term health services.4 Most of the research has focused mainly on chronic morbidities such as neurodevelopmental outcomes, bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), and cognitive abilities.4 Dental health issues related to prematurity include enamel hypoplasia
of primary teeth, which can lead to increased susceptibility to early childhood caries (ECC).5 From the 1Department of Pediatrics, Division of Neonatology, MetroHealth Medical Center and Case Western Reserve University, Cleveland, Ohio, USA; 2Department of Pediatrics, Division of Neonatology, University of Louisville, Louisville, Kentucky, USA; and 3 Department of Community Dentistry, School of Dental Medicine, Case Western Reserve University, Cleveland, Ohio, USA. Financial disclosure: This study was supported by National Institutes of Health grant R01DE017947 from the National Institute of Dental and Craniofacial Research and by CTSC UL1RR024989 and CTSC UL1TR000439 from the National Center for Research Resources. Conflict of interest: The authors declare no conflict of interest. Supplementary material for this article is available on the Journal of Parenteral and Enteral Nutrition website at http://jpen.sagepub.com/ supplemental. Received for publication November 7, 2014; accepted for publication January 19, 2015. Corresponding Author: Roula Merheb, MD, Department of Pediatrics, Division of Neonatology, MetroHealth Medical Center and Case Western Reserve University, 2500 Metro Health Drive, Cleveland, OH, 44109, USA. Email: [email protected].
Downloaded from pen.sagepub.com at University of Otago Library on July 18, 2015
2
Journal of Parenteral and Enteral Nutrition XX(X) mineralization of the enamel. Other comorbidities such as osteopenia, sepsis, patent ductus arteriosus (PDA), and intraventricular hemorrhage (IVH) during the neonatal period can negatively affect the absorption and metabolism of nutrients supply.20 To our knowledge, there are no studies that have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. We hypothesize that VLBW infants with enamel defects would have poorer nutrition status compared with VLBW infants without enamel defects. Thus, the objective of the study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects.
Figure 1. Enamel hypoplasia in the teeth of infants.
Subjects and Methods Enamel is a unique hard tissue in that it does not remodel. It is formed by mineralization of a protein matrix, which begins at about 14–15 weeks of gestation in utero and continues until late adolescence.6 Any insults during this period result in developmental defects of enamel (DDE), which consist of enamel hypoplasia and/or diffuse opacity and/or demarcated enamel.7 DDE is mainly caused by a dysregulation in calcium homeostasis resulting from systemic causes prenatally or postnatally and/or local causes such as endotracheal intubation in the postnatal period.8 Enamel hypoplasia is a common quantitative tooth defect in which there is a deficient amount of enamel, often resulting in discoloration and caries susceptibility9 (Figure 1). It is a biological marker for intrauterine stress, and in recent studies, it has been shown that individuals who had enamel hypoplasia in the neonatal period tend to be subject to earlier adolescent or adult mortality.10 Enamel opacity is another tooth defect that is defined as a qualitative change in the translucency of the enamel.11 Previous studies have described a higher prevalence of DDE in preterm patients with low birth weight (LBW;
