Enamel defects of the primary dentition and osteopenia of prematurity.

Enamel formation (amelogenesis) in the human dentition begins in utero. The process has been investigated widely in the primary dentition in animals, and to a much lesser extent in humans. Studies have confirmed that amelogenesis occurs in distinct stages. 1 Each of these stages may be affected by extreme systemic physiological changes with hypoplasia, hypomineralization, or opacities of enamel. Mineralization begins at 15-21 weeks in intrauterine life in the incisor teeth, at 19-22 weeks in the canines, and at 16-22 weeks in the molars. Major disturbances before, or in the early period after birth may be reflected in the enamel of the primary dentition. Skeletal mineralization in utero is maximal in the last trimester. Of the 30 g of calcium typically present in the term infant’s skeleton, 25 g will be laid down in this trimester. Calcium is deposited chiefly as hydroxyapatite. The higher rate of calcium accretion during this period of calcium deposition in the skeleton, and part of the period of enamel calcification of the primary teeth overlap. Following premature birth the infant is unable to match the intrauterine accretion rate of calcium, which predominantly resides in the skeleton. Indeed calcium intakes often only average 75 mg/ kg/day, compared with the in utero accretion rate of 120-150 mg/kg/day. The level of skeletal mineralization can be assessed using photon absorptiometry at a single peripheral skeletal site. 2 This technique has demonstrated that infants of fewer than 32 weeks gestation at birth have gross reductions in bone mineral content (BMC) upon reaching full-term when compared with those born full-term. ~ Reductions in BMC have been found to be approximately 40-50% when related to age. Enamel defects in primary teeth have been described in preterm infants and have been linked to disorders of calcium metabolism, particularly to premature neonatal hypocalcemia, Vitamin D dependency rickets, or hypoparathyroidism.4, 5 A study of 106 children born prematurely found enamel hypoplasia in 37%, chiefly in the maxillary incisors. 6 Seow et al. 7 showed that in very-low-birth-weight (< 1500 g) prematurely born children, the prevalence of enamel hypoplasia was 62.3%, and 27.3% in low birth weight (1500-2500 g) children, compared with 12.8% in controls. No one factor could be related to the primary tooth enamel hypoplasia, but laryngoscopy and orotracheal intubation also may contribute to developmental defects of the upper anterior primary teeth. 8-11 Early hypocalcemia is a poor guide to neonatal calcium homeostasis, since it is almost universal in preterm infants and is also temporary in nature. The question arose as to whether enamel defects -namely defects in dietary mineral supply -are related to osteopenia of prematurity, and whether a measure of the degree of osteopenia could be used to predict enamel defects. The purpose of this present study was to examine the relationship between enamel defects in the primary dentition and BMC in premature infants.