Enamel defects in prematurely born, low birth-weight infants.

The purpose of this study was to relate the influence of birth and metabolic parameters of the low birth-weight neonate to the development of the primary teeth. The role of hypocalcemia as a specific determinant of enamel hypoplasia was examined. A total of 106 low birth-weight children ranging in age from 18 months to 8 years were examined to determine the frequency of enamel defects. Enamel hypoplasia was found in primary maxillary incisors in 38% of the sample; enamel hypocalcification on maxillary permanent incisors affected 58% of the smnple. The relationship between enamel hypoplasia and plastna calcium was not statistically significant; several mitigating factors are discussed. However, those neonates with low calcium readings had significantly lower birth weights, shorter birth lengths, lower gestational ages, lower 1-min Apgar scores, lower ad~nission temperature, and longer time to regain birth weight than those with no low calcium readings. The high prevalence of enamel hypocalcification in the permanent teeth was speculated to be the result of ~netabolic stresses during the first few months postterm. This study showed no correlation between enamel hypocalcification and the birth parameters. Premature birtlhs (gestation age less than 37 weeks) account for 7-10% of all live births. Prematurely born children are subject to a variety of metabolic stresses and therefore provide an opportunity for studying the effect of severe metabolic parameters on both development and the eruption of teeth. In this paper the prevalence of enamel hypoplasia and hypocalcification and possible etiologic factors are considered. While the specific biochemical cause of enamel hypoplasia has not been determined, there has been growing evidence in recent years that enamel hypoplasia is linked to calcium homeostasis. This hypothesis is based on reports of a high prevalence of enamel hypoplasia in children who have pediatric disturbances such as neonatal tetany, vitamin D-dependent rickets (VDDR), simple rickets, renal disease, and cerebral palsy, and also in infants of diabetic mothers. ~-s The prevalence of enamel hypoplasia in the prematurely born has been reported at between 18 and 43%.9"~° The metabolic factor common to all these conditions is episodes of hypocalcemia. Several studies suggest a direct relationship between enamel hypoplasia in primary teeth and neonatal hypocalcemia. Stimmler et al. ~1 studied 12 children who had severe late neonatal hypocalcemia with convulsions during the fifth to tenth day of life. All had brown bands of hypoplastic lesions on the primary canines and molars. In most cases the primary central and lateral teeth were not affected; this was attributed to crown completion before the onset of the hypocalcemia. They reported that the observed abnormalities were not characteristic of those found in the prematurely born children as reported by Miller and Forrester 3 or Sarnat and Schour. 12,13 However, in children with hypocalcemia associated with congenital hypoparathyroidism, the enamel hypoplasia had characteristics similar to lesions observed in prematurely born infants. Purvis et al. ~4 histologically examined primary teeth with similar enamel hypoplastic defects and suggested that the condition might have been produced by a vitamin D deficiency during pregnancy and further aggravated by reduced exposure to sunlight during winter months, thereby producing secondary hyperparathyroidism in the mother. This was challenged by Stimmler et al. ~s who maintained that the enamel defects were caused postnatally rather than prenatally. 218 ENAMEL DEFECTS/INFANTS: Pimlott et al. TABLE 1. Prevalence of Enamel Hypoplasia and Hypocalcification in Low Birth-weight, Prematurely Born Children A. Enamel Hypoplasia Number % PreTooth of valence Gingival Either Arch Teeth Numbers Children Incisal Half Half Half Maxillary Medial incisors 51, 61 72 35’ 5~ 36 Lateral incisors 52, 62 87 33 3 34 Any incisors 51, 52, 87 37 3 38 61, 62 Canines 53, 63 101 8 0 8 1st molars 54, 64 103 3 1 3 2nd molars 55, 65 82 2 0 2 Any posterior 53, 54, 55, 104 11 1 11 63, 64, 65 Mandibular Medial incisors 71, 81 48 4 0 4 Lateral incisors 72, 82 70 3 0 3 Any incisors 71, 72, 81, 82 71 4 0 4 Canines 73, 83 98 2 1 3 1st molars 74, 84 104 3 2 3 2nd molars 75, 85 82 4 0 4 Any posterior 73, 74, 75, 105 6 3 8 83, 84, 85 Either arch any tooth 106 37 B. Enamel hypocalcification Premature Sample Normal Sample Number Number of % Preof % PreArch Teeth Tooth Numbers Children valence Children valence Maxillary Medial incisors 11, 21 37 59 40 8 Lateral incisors 12, 22 17 12 --This percentage is based on 71 children instead of 72, as the medial incisors of 1 child were so worn that the incisal half could not be assessed. This percentage is based on 66 children instead of 72, as the medial incisors of 6 children were erupted only partially and the gingival half was not visible. Levine and Keen~6 examined histologically and microradiographically 25 primary teeth of children with neonatal hypocalcemia. They found no evidence to suggest that the defect was caused prenatally as Purvis et al. 14 had indicated. However, they found that the appearance of the hypoplastic lesion was similar to those reported in two other conditions: kernicterus 3 and cerebral palsy. ~7,18 Noren et al. 7 found an increased prevalence of enamel hypoplasia in infants of diabetic mothers. They speculated that these enamel defects were due to functional hypoparathyroidism which resulted in states of hypocalcemia and hyperphosphatemia. In a definitive study of children with chronic disorders of calcium and phosphorus homeostasis, Nikiforuk and Fraser 8 found enamel hypoplasia in those conditions where hypocalcemia existed (e.g., hereditary VDDR and hypoparathyroidism), but not in those conditions with hypophosphatemia and normal calcium levels (x-linked hypophosphatemic rickets). Therefore, they concluded that enamel hypoplasia was not related to plasma phosphorus levels, but rather to hypocalcemia during the development of the teeth. The purpose of the present study was to relate the influence of birth and metabolic parameters (especially hypocalcemia) in prematurely born, low birthweight neonates on the development of their primary teeth. Methods and Patient Sample In this study all children were born prematurely (gestational age < 37 weeks) and had birth weights < 1500 g. All were enrolled in the prenatal follow-up program at the Hospital for Sick Children in Toronto. A total of 106 children (57 males, 49 females) ranging in age from 18 months to 8 years were studied by a single examiner to determine the frequency of enamel defects, specifically enamel hypoplasia and enamel hypocalcification. Enamel hypoplasia was defined as a quantitative defect in the enamel surface, while enamel hypocalcification was defined as the presence PEDIATRIC DENTISTRY: September 1985/Vol. 7 No. 3 219 TABLE 2. t-Tests of Differences in Birth Variables Between Enamel Hypoplasia Groups and Between Lowest Serum Calcium Groups Birth Variable Enamel Hypoplasia YES NO Birth Mean 1119 1128 Weight SD 233 217 (g) n 33 54 p .85 Birth Mean 35.83 37.54 Length SD 4.28 2.37 (cm) n 32 53 p .04* Birth Mean 27.55 26.25 Head SD 5.24 2.10 Circumf. n 32 53 (cm) p .19" Lowest Serum Calcium <6 mg/100 ml~>6 mg/100 ml 1027 1167 199 212 32 71 .0O2 35.65 37.40 3.43 2.85 31 69 .009 26.57 26.61 3.90 3.22 31 69 .95 Gestationa] Age: Clinical (weeks Mean 29.97 30.02 SD 2.14 2.81 n 31 51 p .93 28.94 30.38 1.98 2.62 31 66 .008 Apgar Mean 4.69 4.40 Score: SD 2.39 2.51 1 rain n 29 48 p .61 Apgar Mean 6.44 6.70 Score: SD 2.85 2.48 5 rain n 27 46 p .69 Admission Temp. (°C) Mean 36.18 35.86 SD 1.19 1.11 n 32 52 p .24 Days to Mean Regain SD Birth n Weight p * T-test for unequal variances. 3.52 4.82 1.96 2.6O 25 60 .O3 6.21 6.57 2.89 2.45 24 56 .56 35.45 36.10 1.06 1.12 30 69 .008 19.43 21.64 8.53 11.43 30 48 .36 25.15 19.85 10.39 9.71 26 65 .O2 of an area of enamel exhibiting a distinct white opalescence with no detectable structural defect. In addition, a control sample of 40 full-term children was examined for the presence of enamel hypocalcification. The children resided in an area where the water supply contained l ppm fluoride; no subject reported receiving fluoride supplements. Data regarding birth parameters for each child were gathered. These included: birth weight; birth Iength; birth head circumference; gestational age; Apgar scores; pH at birth; temperature at birth; time to regain birth weight; and the presence of absence of asphyxia, apnea, and convulsions at birth. Plasma calcium readings during the first week of life also were obtained, as well as data pertaining to the growth of these children up to the age of 2 years.