Although many studies have discussed health risks in neonates with a low birth weight, few studies have focused on the risks in neonates with a high birth weight. The objective of this study was to determine whether differences in the incidence of dental caries in early childhood are associated with birth weight status.
A total of 117,175 children born in Okinawa Prefecture, Japan from 1997 to 2007 were included in this study. Medical professionals collected information about birth records, growth and development, parental child-rearing practices and dental health at 3 months, 18 months and 3 years of age. The risk of dental caries among neonates with macrosomia (birth weight ≥4000 g) was compared with that among neonates with normal weight (2500–3999 g). Sensitivity analyses included ‘large for gestational age’ (LGA, birth weight above the 90th percentile for gestational age), which was relative to ‘appropriate for gestational age’ (birth weight between 10th and 90th percentiles). Relative risks and relative risk increases were estimated by multivariate Poisson regression.
At 3 years of age, the relative risk increases for dental caries after adjusting for confounding factors were 19% [95% confidence interval (CI), 11%–28%, P < 0.001] for macrosomic neonates and 12% (95% CI, 9%–16%, P < 0.001) for LGA neonates.
Citation: Yokomichi H, Tanaka T, Suzuki K, Akiyama T, Okinawa Child Health Study Group, Yamagata Z (2015) Macrosomic Neonates Carry Increased Risk of Dental Caries in Early Childhood: Findings from a Cohort Study, the Okinawa Child Health Study, Japan. PLoS ONE 10(7): e0133872. https://doi.org/10.1371/journal.pone.0133872
Editor: Karin Bammann, University of Bremen, GERMANY
Received: February 6, 2015; Accepted: July 3, 2015; Published: July 24, 2015
Copyright: © 2015 Yokomichi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Data Availability: Due to ethical restrictions, data are available upon request from Professor Zentaro Yamagata (firstname.lastname@example.org).
Funding: This work was supported by the Ministry of Health, Labour and Welfare of Japan [Jisedai-Ippan (H25-002, http://www.mhlw.go.jp/seisakunitsuite/bunya/hokabunya/kenkyujigyou/hojokin-koubo-h25/gaiyo/08.html) to ZY] and by the Ministry of Education, Culture, Sports, Science and Technology of Japan [Grant-in-Aid for Young Scientists (B) (24790614, https://kaken.nii.ac.jp/d/p/24790614.en.html) and Grant-in-Aid for Scientific Research (C) (15K08730, https://kaken.nii.ac.jp/d/p/15K08730.en.html) to HY]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Difficulties experienced during pregnancy and childbirth form the subject of on-going clinical and basic research worldwide. Children born to obese mothers exhibit increased rates of childhood obesity and subsequent paediatric lifestyle-related diseases;[1, 2] furthermore, a controlled maternal weight at birth reduces the risk of adulthood obesity.[3–6] Although numerous available studies have evaluated low birth weight as a risk factor for growth retardation, metabolic syndrome, early puberty and attention-deficit hyperactive disorder (ADHD), few have report the risks associated with macrosomia. Moreover, macrosomic infants are not carefully monitored.
The potential risk factors and preventive factors associated with paediatric dental caries include hypoplastic enamel, early dental eruption, dental hygiene (brushing the teeth by parents, fluoridated water ), excess consumption of sweets, prolonged breastfeeding, prolonged nursing with a bottle, irregular consumption of meals and snacks, insufficient dietary calcium in both the mother and child, low parental socioeconomic status, parental smoking[16, 17] and support for child rearing. Although all of these environmental and genetic factors are potentially causative or preventative candidates in terms of caries, the neonatal size has not been considered in these studies, despite its potential impact on the child’s dental health.
Although considerable research has been undertaken to determine whether caries are associated with obesity, previous reports have been unable to end the controversy because of confounding factors. In particular, the association between obesity in toddlerhood and caries in primary teeth remains inconclusive. Similarly, whether a low birth weight is a protective or risk factor for dental caries remains controversial.[21, 22] Moreover, there are no published data on the incidence of dental caries among neonates with high birth weights. Only one cohort study in the United Kingdom reported a small linear relationship between the caries incidence and birth weights ranging from low to high (odds ratio = 1.08 per 100 g of birth weight); however, this relationship was not significant. In the previous study, the number of enrolled children was limited to 985, and the applied linear regression analysis did not investigate the possible J-shaped caries risk from low to high birth weights. Therefore, we aimed to determine whether a high birth weight was associated with the incidence of dental caries in primary teeth in a large population, simultaneously considering many risk factors associated with caries.
The Ethics Review Committee of the Faculty of Medicine of the University of Yamanashi approved the study protocol in accordance with the ethical guidelines and regulations of the Declaration of Helsinki. The Japanese guidelines permit the use of data from medical examinations without consent if the data are anonymous; therefore, informed consent was not required for the current investigation.
Study design and participants
The Okinawa Child Study is a cohort study based on the free health examinations provided to children by administrative authorities. More than 82% of the approximately 16,000 children born annually in Okinawa participate in these health examinations at 3 months, 18 months and 3 years of age. The present study was conducted using data from participants born between 2 April 1997 and 1 April 2007 (i.e. Japanese school years from 1997 to 2006). In this study, data from children who lacked birth records, medical records or oral health records were excluded.
Data regarding birth records, family composition, parental child-rearing practices, dietary habits and dental examinations were collected from the child health examinations. We analysed data for the following variables: sex, birth weight, gestational age, parity, siblings, children’s dental hygiene, children’s history of dental fluoridation, use of a bottle for nursing, consumption of cow’s milk and snacks, parental age, parental occupation, parental smoking habits and people involved in child-rearing. Qualified public health nurses and paediatricians performed all examinations for determining parental child-rearing practices, anthropometrics, growth and development. Qualified dentists evaluated the children’s oral health and diagnosed dental caries. Each child underwent this dental examination conducted by an on-site dentist. During the paediatric health examinations, the public health nurses interviewed mothers regarding their child-rearing practices. Macrosomia, normal birth weight and low birth weight were defined as birth weights of ≥4000 g,[26–29] 2500–3999 g and <2500 g, respectively, in accordance with the standards of the World Health Organization. The definitions of ‘large for gestational age’ (LGA), ‘appropriate for gestational age’ (AGA) and ‘small for gestational age’ (SGA) were weights above the 90th percentile, between the 10th and 90th percentiles and below the 10th percentile for gestational age, respectively.[31, 32] Herein, birth weight reference categories used to compare the risk of caries were normal birth weight and AGA.
The risks of having caries at 3 years of age among neonates with macrosomia and low birth weights were compared with the risks in other neonates. Multivariate Poisson regressions were used to estimate the relative risks (RR) with respect to the controlled confounding factors, as odds ratios tend to misrepresent the risks of exposure for high prevalence or incidence.[33, 34] RRs were determined for the following explanatory variables: sex, birth weight, mother’s age, gestational age, birth order, the number of teeth at 18 months, parents’ employment status, use of a bottle for nursing at 18 months, dental fluoridation, siblings, parental smoking, brushing the teeth by parents at 18 months and 3 years of age, drinking cow’s milk at 18 months and 3 years of age, eating irregular meals and snacks at 18 months and 3 years of age and watching TV or videos. Although some literature suggests breastfeeding as a risk factor of dental caries, as a cultural norm, Japanese paediatricians and domestic public health nurses encourage mothers to begin ablactating at 5–6 months and to finish by the time their child is 18 months age. Therefore, breastfeeding and ablactating were not considered confounding factors for dental caries at 3 years of age. Regarding the use of pacifiers, the Japanese Society of Pediatric Dentistry and Japanese mothers are aware of the risks of interrupted normal bite resulting from pacifier use. As a result, the proportion of pacifier use is low; therefore, we did not consider it to be a confounding factor in Japan. Relative risk increases (RRI) were calculated as RR − 1. Furthermore, we calculated the adjusted least square estimates of the number of decayed or filled teeth to assess the marginal means over a population that had been adjusted according to other explanatory variables in a multivariable regression. Descriptive statistical analyses and estimations of RRs were performed using SAS statistical software (version 9.3, SAS Institute, Cary, NC, USA). Descriptive statistics are reported as means and standard deviations (SDs), and point estimates are reported with 95% confidence intervals (CI). All reported P values are 2-sided, and a P-value <0.05 was considered statistically significant.
The United States Preventive Service Task Force and American Academy of Pediatrics recommend that fluoride varnish treatment should begin with primary tooth eruption.[38, 39] Accordingly, we believed that previous clinical fluoridation of primary teeth might have modified the risks, and therefore previous use of fluoride varnish was included in the first sensitivity analysis; this was restricted to the school years of 2006 and 2007, when detailed records of previous clinical fluoride varnish treatment were preserved. The second sensitivity analysis included LGA, AGA and SGA instead of macrosomia, normal birth weight and low birth weight, respectively; LGA, AGA and SGA were applied to the subjects who were evaluated according to the standards for Japanese children in the guidelines of Japan Obstetrics and Gynaecology. In the third sensitivity analysis, the included children were restricted to those born through labour at term (i.e. gestational age of 37–41 weeks); accordingly, children born through pre- and post-term deliveries were excluded to minimize the result of exposure on the outcome, as gestational age may be associated with an earlier or later eruption of teeth susceptible to caries. Fourth, multivariate analyses of the association between macrosomia and dental caries were performed in the school years 1997–1999, 2000–2002 and 2003–2006 to explore how secular changes in diet contributed to the results. In all sensitivity analyses, multivariate Poisson regressions to adjust for confounding factors were conducted in the same manner used for the main analysis.
Among the 117,651 participants who underwent the health examination and for whom demographic data were available, we excluded 476 children who were toothless at 3 years of age, leaving a final sample size of 117,175. Table 1 shows the following mean demographic values among the population with 60,167 (51.4%) male subjects: birth weight, 3014 g (SD, 434); gestational age, 38.0 weeks (SD, 5.6); age of the mother at the 3-month examination, 29.7 years (SD, 5.6); birth order, 1.9 (SD, 1.0) and number of teeth at 18 months of age, 14.5 (SD, 2.7). Dental caries were present in 53,924 children (46.0%) at 3 years of age, and 1266 children (1.1%) were born with macrosomia.
On univariate analysis, the risk of having caries at 3 years of age was significantly higher among children with macrosomia relative to those with normal birth weights (RRI, 23%, CI, 18–29, P < 0.001). Other univariate analyses yielded the following RRIs: 19% (CI, 17–21, P < 0.001) for a maternal age <25 years, 7% (CI, 0.01–14, P = 0.0496) for post-term delivery, 21% (CI, 19–22, P < 0.001) for non-firstborn babies, 14% (CI, 12–16, P < 0.001) for ≥14 teeth at 18 months of age, 22% (CI, 19–25, P < 0.001) for unemployed parents, 21% (CI, 19–23, P < 0.001) for maternal or paternal smoking, −5% (CI, −6–−3, P < 0.001) for no siblings at 3 years of age, 27% (CI, 23–31, P < 0.001) for no support for child rearing, 40% (CI, 38–42, P < 0.001) for occasional brushing the teeth by parents at 3 years of age, −19% (CI, −20–−18, P < 0.001) for drinking cow’s milk and 32% (CI, 30–34, P < 0.001) for irregular consumption of meals and snacks at 18 months of age (Table 2).
Relative risk increase equals relative risk minus 1.
The following RRIs were obtained through the main multivariate regression: 19% (CI, 11–28, P < 0.001) for macrosomic babies, 17% (CI, 14–20, P < 0.001) for a maternal age <25 years, 7% (CI, −3–18, P = 0.21) for post-term delivery, 26% (CI, 24–29, P < 0.001) for non-firstborn babies, 11% (CI, 6–16, P < 0.001) for unemployed parents, 15% (CI, 13–17, P < 0.001) for maternal or paternal smoking, 17% (CI, 13–22, P < 0.001) for no support for child rearing, 22% (CI, 19–25, P < 0.001) for occasional brushing the teeth by parents at 3 years of age, −12% (CI, −14–−10, P < 0.001) for drinking cow’s milk and 16% (CI, 13–18, P < 0.001) for irregular consumption of meals and snacks at 18 months of age (Table 2).
The first sensitivity analysis, which was adjusted for previous clinical fluoride varnish treatment, estimated the RRIs for macrosomic birth weight and the effect of fluoridation on the incidence of caries at 3 years of age to be 4% (CI, −17–30, P = 0.72) and 4% (CI, −2–9, P = 0.16), respectively. In the second sensitivity analysis, the estimated RRIs for LGA and SGA were 12% (CI, 9–16, P < 0.001) and −1% (CI, −4–2, P = 0.49), respectively. In the third sensitivity analysis, which was restricted to children born via labour at term, the RRI of a macrosomic birth weight for caries at 3 years of age was 19% (CI, 11–28, P < 0.001). In the fourth sensitivity analysis, the estimated RRIs for macrosomia were 20% (CI, 6–36, P < 0.01) during 1997–1999, 17% (CI, 4–32, P < 0.01) during 2000–2002 and 16% (CI, 3–30, P = 0.01) during 2003–2007.
Among macrosomic children, the RRI of caries at 3 years of age was 19%, representing a significant increase relative to children with normal birth weights. Four sensitivity analyses, which considered the clinical use of fluoride varnish, LGA, labour at term and secular trends, yielded approximately the same RRIs for children with high birth weights.
Possible reasons for these associations
Although the mechanism underlying the formation of caries after exposure to intrauterine over-nutrition is not understood, relatively high concentrations of glucose and amino acids in utero may increase the postnatal appetite or insulin secretion. Evidence indicates that overweight pregnant women have high concentrations of inflammatory cytokines and increased insulin resistance, and subsequently compensatory hyperinsulinaemia and foetal adiposity occur in utero.[41, 42] Hoegsberg et al. observed that macrosomic neonates of nondiabetic mothers are more likely to exhibit hyperinsulinaemia than normal size neonates. Moreover, in foetal rhesus monkeys, external insulin injection resulted in the delivery of macrosomic neonates with hyperinsulinaemia. Dörner et al. suggested that perinatal hyperinsulinaemia alters the function of hypothalamic ventromedial nuclei, which play a determining role in satiety, appetite and insulin secretion from pancreatic β-cells. Studies in rats have revealed foetal β-cell hyperplasia in the offspring of moderately diabetic mothers.[46, 47] The ‘Developmental over-nutrition hypothesis’, which was recently submitted based on animal model studies, proposes that maternal nutritional and hormonal conditions during pregnancy programme the appetite and energy expenditure of the offspring, as well as the hormonal, neuronal and autocrine mechanisms that contribute to the offspring’s energy balance. Thereafter, the primary teeth of LGA children may be more frequently exposed to cariogenic food and drink than the teeth of AGA children. Furthermore, the finding that LGA neonates remain classified as overweight until the age of 83 months[49, 50] might reflect the hypothetical programming in utero and subsequent voracious appetite.
Comparison with other studies
Regarding the positive effect of macrosomia on dental caries, we have calculated the following: if the previous report from the UK regarding a small positive association between birth weight and the risk of caries (odds ratio (OR) = 1.08 per 100 g of birth weight) could be directly applied to 4000 g (lower limit of macrosomia) with a reference of, for instance, 3000 g, the OR may be calculated as 2.16 [i.e. 1.08 to the 10th power, where 10 equals (4000−3000)/100]; the calculated OR is mathematically equivalent to a RR of 1.41 and RRI of 41%, given that the risk of caries was 46% among children born at a weight of 3000 g. Therefore, our estimated RRI = 19% was not overly large, and we consider our result to be consistent with the previous study. Regarding the negative RRI of −5% for a low birth weight, our results were similarly consistent with the above-described report from the UK. In addition, Saraiva et al. suggested that SGA, foetal growth restriction and pre-term birth should be associated with a lower incidence of dental caries among Caucasian, African-American and Mexican-American children aged 2–5.9 years. Our results regarding low birth weight and SGA provided evidence from a Japanese population to support the findings of Saraiva et al. A programmed lower appetite, as discussed above, might explain these observations related to the lower incidence of caries in children with low birth weights.
In the first sensitivity analysis, which was restricted to data from 2 school years and included the clinical use of fluoride varnish, the RRI adjusted for previous fluoride varnish use was 4% (CI, −17–30, P = 0.72), with a lower result in the main multivariate analysis. Taking the large CI and non-significance into account, we considered that these data related to fluoride varnish use were unreliable for estimating the effect of macrosomia. In other words, in an era when almost all commercial fluoridated dental toothpastes contain fluoride and dental clinics and individual dentists routinely apply fluoride rinses, gels or varnishes to the primary teeth during paid clinical examinations, we do not consider previous fluoride varnish use to be an important confounding factor in the present study. The paradoxical effect of previous clinical fluoride varnish use, which has an RRI of 4% (CI, −2–9, P = 0.16), may represent the uselessness of this information in the present-day survey.
In the second sensitivity analysis, in which our exposure variable of interest was changed from rare macrosomia (birth weight ≥4000 g) to LGA, the RRI of LGA for caries development (12%) was similar to that of macrosomia (19%); in addition, the relatively lower RRI associated with LGA can be reasonably explained by the fact that LGA is, by definition, more frequent than macrosomia. It should be emphasized that the third sensitivity analysis, which excluded children born via pre- and post-term delivery and was therefore restricted to those born through labour at term, yielded the same RRI of 19%. Because the timing of tooth eruption and the number of susceptible teeth among term neonates are considered to be approximately the same, this sensitivity analysis confirmed our report regarding the effect of macrosomia on dental caries in early childhood. Moreover, the fourth sensitivity analysis confirmed the RRI of macrosomia in recent years as 16–20%.
Strengths and limitations
To the best of our knowledge, this is the first report to raise an alarm over the risk of a high birth weight with respect to dental caries of the primary teeth. A study in the UK suggested a weak linear relationship between incidental caries and birth weights ranging from low to high, but that previous study could not clarify the risk of macrosomia by its linear regression analysis. In this study, we used birth weights as a categorical variable to examine whether both high and low birth weights are risk factors for dental caries (J-shaped risk); however, the results were not similar to those of the previous study. Second, our large amount of data obtained from the free health service provided to resident children by the administrative authorities retained sufficient statistical power to determine the risks of a high birth weight, whereas the data set in the previous study in the UK also lacked statistical power. Third, the sensitivity analyses confirmed the postulated risk of macrosomia. Furthermore, the measurements were valid because all of the health professionals were qualified to evaluate caries, anthropometrics and interviews addressing parental child-rearing practices and several socioeconomic statuses.
One limitation of this study was the lack of available information about parental dental hygiene and typical socioeconomic status. Parental self-dental care may have directly affected the incidence of caries in their children. However, because parental lifestyles and dental hygiene are reflected by the socioeconomic status, this potential confounding bias might have been reduced by adjusting for information regarding the parental employment status, smoking habits, siblings, child-rearing support provided by others, parental support for brushing their children’s teeth and irregular consumption of meals and snacks. Another limitation in interpreting the results would be that the dental caries were neither validated by other dentists nor validated for different periods of time. Owing to the nature of administrative massive health examinations, the number of on-site dentists is limited. Because there is no published data describing the likelihood of dental caries diagnosis at health examination centres compared to that at dental clinics, the influence of lack of validation on the number of diagnosed caries in this report is unknown. However, even if a misclassification of children with and without caries existed, dentists were unlikely to diagnose caries in view of child birth weights; therefore, we believe that the bias because of this influence in the reported RRIs would be minimal. The other potential limitation of this study is its regional restriction to Okinawa; therefore, the results may not be applicable to other regions of Japan. Moreover, during the study period, approximately 25% of children in Okinawa did not undergo health examinations or were excluded from the study because of insufficient information. It is possible that these missing children had poor access to health examinations and were born to families with low socioeconomic statuses. As a result, the frequencies of high birth weight and caries in that population might have exceeded those of the children studied, and accordingly the missing data might have biased the RRIs of our results.
Implications and conclusions
To the best of our knowledge, we are the first to report that macrosomia significantly increases the risk of dental caries. Our focus on the influence of high birth weight on this paediatric lifestyle-related disease represents a new perspective in perinatal research. The mechanism of the relationship between macrosomia and dental caries remains under debate, and further laboratory and clinical studies are warranted. We recommend that children with macrosomia should receive close attention from medical professionals during development.
The steering committee of the Okinawa Child Health Study Group includes Drs Y. Anri, T. Nakasone, T. Tomima, K. Katsuren, E. Kuniyoshi, H. Tamaki, C. Hika, E. Tamanara, Y. Shimoji, M. Kohama, H. Hamahashi, S. Takara and Y. Hayashi.
Conceived and designed the experiments: ZY. Performed the experiments: HY TT KS TA. Analyzed the data: HY. Contributed reagents/materials/analysis tools: TT KS. Wrote the paper: HY ZY KS.
- 1. Strauss RS, Knight J. Influence of the home environment on the development of obesity in children. Pediatrics. 1999;103:e85. pmid:10353982
- 2. Reynolds RM, Allan KM, Raja EA, Bhattacharya S, McNeill G, Hannaford PC, et al. Maternal obesity during pregnancy and premature mortality from cardiovascular event in adult offspring: follow-up of 1 323 275 person years. BMJ. 2013;347:f4539. pmid:23943697
- 3. Hochner H, Friedlander Y, Calderon-Margalit R, Meiner V, Sagy Y, Avgil-Tsadok M, et al. Associations of maternal prepregnancy body mass index and gestational weight gain with adult offspring cardiometabolic risk factors: the Jerusalem Perinatal Family Follow-Up Study. Circulation. 2012;125:1381–9. pmid:22344037
- 4. Fraser A, Tilling K, Macdonald-Wallis C, Sattar N, Brion MJ, Benfield L, et al. Association of maternal weight gain in pregnancy with offspring obesity and metabolic and vascular traits in childhood. Circulation. 2010;121:2557–64. pmid:20516377
- 5. Lawlor DA, Lichtenstein P, Fraser A, Langstrom N. Does maternal weight gain in pregnancy have long-term effects on offspring adiposity? A sibling study in a prospective cohort of 146,894 men from 136,050 families. Am J Clin Nutr. 2011;94:142–8. pmid:21562086
- 6. Reynolds R, Osmond C, Phillips D, Godfrey K. Maternal BMI, parity, and pregnancy weight gain: influences on offspring adiposity in young adulthood. J Clin Endocrinol Metab. 2010;95:5365–9. pmid:20702520
- 7. Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics. 2005;115:e290–e296. pmid:15741354
- 8. Hack M, Youngstrom EA, Cartar L, Schluchter M, Taylor HG, Flannery D, et al. Behavioral outcomes and evidence of psychopathology among very low birth weight infants at age 20 years. Pediatrics. 2004;114:932–40. pmid:15466087
- 9. Lai P, Kim Seow W, Tudehope D, Rogers Y. Enamel hypoplasia and dental caries in very-low birthweight children: a case-controlled, longitudinal study. Pediatr Dent. 1997;19:42–9. pmid:9048413
- 10. McDonagh MS, Whiting PF, Wilson PM, Sutton AJ, Chestnutt I, Cooper J, et al. Systematic review of water fluoridation. Brit Med J. 2000;321:855–9. pmid:11021861
- 11. Gibson S, Williams S. Dental caries in pre-school children: associations with social class, toothbrushing habit and consumption of sugars and sugar-containing foods. Further analysis of data from the National Diet and Nutrition Survey of children aged 1.5–4.5 years. Caries Res. 1999;33:101–13. pmid:9892777
- 12. Iida H, Auinger P, Billings RJ, Weitzman M. Association between infant breastfeeding and early childhood caries in the United States. Pediatrics. 2007;120:e944–e952. pmid:17908749
- 13. Anderson TD. American Academy of Pediatrics: Soft Drinks in Schools. Pediatrics. 2004;113:152–4. pmid:14702469
- 14. Ji Y, Du X, Okazaki Y, Hori M, Yamanaka K, Mori Y, et al. Risk behaviors and its association with caries activity and dental caries in Japanese children. Pediatr Dent J. 2006;16:91–5.
- 15. Warren JJ, Weber‐Gasparoni K, Marshall TA, Drake DR, Dehkordi‐Vakil F, Dawson DV, et al. A longitudinal study of dental caries risk among very young low SES children. Community Dent Oral. 2009;37:116–22.
- 16. Aligne CA, Moss ME, Auinger P, Weitzman M. Association of pediatric dental caries with passive smoking. JAMA. 2003;289:1258–64. pmid:12633187
- 17. Tanaka K, Miyake Y, Sasaki S. The effect of maternal smoking during pregnancy and postnatal household smoking on dental caries in young children. J Pediatr. 2009;155:410–5. pmid:19555966
- 18. Ohsuka K, Chino N, Nakagaki H, Kataoka I, Oshida Y, Ohsawa I, et al. Analysis of risk factors for dental caries in infants: a comparison between urban and rural areas. Environ Health Prev Med. 2009;14:103–10. pmid:19568854
- 19. Kantovitz KR, Pascon FM, Rontani RMP, Gaviao MBD. Obesity and dental caries-A systematic review. Oral Health Prev Dent. 2006;4:137. pmid:16813143
- 20. Hong L, Ahmed A, McCunniff M, Overman P, Mathew M. Obesity and dental caries in children aged 2–6 years in the United States: National Health and Nutrition Examination Survey 1999–2002. J Public Health Dent. 2008;68:227–33. pmid:18384534
- 21. Burt BA, Pai S. Does low birthweight increase the risk of caries? A systematic review. J Dent Educ. 2001;65:1024–7. pmid:11699973
- 22. Shulman JD. Is there an association between low birth weight and caries in the primary dentition? Caries Res. 2005;39:161–7. pmid:15914975
- 23. Kay EJ, Northstone K, Ness A, Duncan K, Crean SJ. Is there a relationship between Birthweight and subsequent growth on the development of Dental Caries at 5 years of age? A cohort study. Community Dent Oral Epidemiol. 2010;38:408–14. pmid:20545719
- 24. Ministry of Health, Labour and Welfare of Japan. Children and Childrearing 2014 [cited 22 June 2015]]. Available://www.mhlw.go.jp/stf/seisakunitsuite/bunya/kodomo/kodomo_kosodate/boshi-hoken/index.html. Japanese.
- 25. The Okinawa Society of Child Health. The Secondary Report of Health Examination for Infants in Okinawa 2014 [cited 22 June 2015]]. Available: http://www.osh.or.jp/. Japanese.
- 26. Boyd ME, Usher RH, McLean FH. Fetal macrosomia: prediction, risks, proposed management. Obstet Gynecol. 1983;61:715–22. pmid:6843930
- 27. Morikawa M, Cho K, Yamada T, Yamada T, Sato S, Minakami H. Fetal macrosomia in Japanese women. J Obstet Gynaecol Res. 2013;39:960–5. pmid:23279000
- 28. Koyanagi A, Zhang J, Dagvadorj A, Hirayama F, Shibuya K, Souza JP, et al. Macrosomia in 23 developing countries: an analysis of a multicountry, facility-based, cross-sectional survey. Lancet. 2013;381:476–83. pmid:23290494
- 29. Boulet SL, Alexander GR, Salihu HM, Pass M. Macrosomic births in the United States: determinants, outcomes, and proposed grades of risk. Am J Obstet Gynecol. 2003;188:1372–8. pmid:12748514
- 30. World Health Organization. Consultation on Definitions and Standards Related to Maternal and Child Health and the Perinatal Period, Washington, DC, 30 March to 3 April 1987: report. 1987.
- 31. Battaglia FC, Lubchenco LO. A practical classification of newborn infants by weight and gestational age. J Pediatrics. 1967;71:159–63.
- 32. Ogawa Y IT, Kuriya N, Kuriya N, Nishida H, Takeuchi H, et al. Birth size standards by gestational age for Japanese neonates. Acta Neonatologica Japonica. 1998;34:624–32. Japanese.
- 33. Zou G. A modified poisson regression approach to prospective studies with binary data. Am J Epidemiol. 2004;159:702–6. pmid:15033648
- 34. Zhang J, Kai FY. What's the relative risk?: A method of correcting the odds ratio in cohort studies of common outcomes. JAMA. 1998;280:1690–1. pmid:9832001
- 35. Harris R, Nicoll AD, Adair PM, Pine CM. Risk factors for dental caries in young children: a systematic review of the literature. Community Dent Health. 2004;21:71–85. pmid:15072476
- 36. Ministry of Health, Labour and Welfare of Japan. Supporting guide for breastfeeding and ablactating. 2007 [cited 22 June 2015]]. Available: http://www.mhlw.go.jp/shingi/2007/03/dl/s0314-17.pdf. Japanese.
- 37. Japanese Society of Pediatric Dentistry. A way of thinking about use of pacifier 2005 [cited 22 June 2015]]. Available: http://www.jspd.or.jp/contents/main/proposal/index03_04.html. Japanese.
- 38. Moyer VA, US Preventive Services Task Force. Prevention of Dental Caries in Children From Birth Through Age 5 Years: US Preventive Services Task Force Recommendation Statement. Pediatrics. 2014;133:1102–11. pmid:24799546
- 39. Kohn WG, Maas WR, Malvitz DM, Presson SM, Shaddix KK. Recommendations for using fluoride to prevent and control dental caries in the United States. MMWR Recomm Rep. 2001;50. (RR-14):1–42
- 40. Ramsay JE, Ferrell WR, Crawford L, Wallace AM, Greer IA, Sattar N. Maternal obesity is associated with dysregulation of metabolic, vascular, and inflammatory pathways. J Clin Endocrinol Metab. 2002;87:4231–7. pmid:12213876
- 41. Catalano PM, Ehrenberg HM. The short- and long-term implications of maternal obesity on the mother and her offspring. BJOG. 2006;113:1126–33. pmid:16827826
- 42. Catalano PM, Presley L, Minium J, Mouzon SHD. Fetuses of Obese Mothers Develop Insulin Resistance in Utero. Diabetes Care. 2009;32:1076–80. pmid:19460915
- 43. Hoegsberg B, Gruppuso PA, Coustan DR. Hyperinsulinemia in macrosomic infants of nondiabetic mothers. Diabetes Care. 1993;16:32–6. pmid:8422801
- 44. Susa JB, McCormick KL, Widness JA, Singer DB, Oh W, Admsons K, et al. Chronic hyperinsulinemia in the fetal rhesus monkey: effects on fetal growth and composition. Diabetes. 1979;28:1058–63. pmid:116897
- 45. Dörner G, Plagemann A. Perinatal hyperinsulinism as possible predisposing factor for diabetes mellitus, obesity and enhanced cardiovascular risk in later life. Horm Metab Res. 1994;26:213–21. pmid:8076902
- 46. Eriksson U, Swenne I. Diabetes in pregnancy: growth of the fetal pancreatic B cells in the rat. Neonatology. 1982;42:239–48.
- 47. Aerts L, Van Assche F. Rat foetal endocrine pancreas in experimental diabetes. J Endocrinol. 1977;73:339–46. pmid:325166
- 48. Taylor PD, Poston L. Developmental programming of obesity in mammals. Exp Physiol. 2007;92:287–98. pmid:17170060
- 49. Hediger ML, Overpeck MD, McGlynn A, Kuczmarski RJ, Maurer KR, Davis WW. Growth and fatness at three to six years of age of children born small-or large-for-gestational age. Pediatrics. 1999;104:e33. pmid:10469816
- 50. Hediger ML, Overpeck MD, Maurer KR, Kuczmarski RJ, McGlynn A, Davis WW. Growth of infants and young children born small or large for gestational age: findings from the Third National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med. 1998;152:1225–31. pmid:9856434
- 51. Saraiva MC, Bettiol H, Barbieri MA, Silva AA. Are intrauterine growth restriction and preterm birth associated with dental caries? Community Dent Oral Epidemiol. 2007;35:364–76 pmid:17822485