Dental Outcomes of Preterm Infants

Diane L. Eastman, MA, RN, CPNP

Disclosures

NAINR. 2003;3(3) 

In This Article

Enamel Defects

Enamel defects are a well-studied complication of prematurity.[3,4,5] Enamel is a hard tissue that once formed, unlike bone, does not remodel. For that reason, insults during enamel development are permanent on the tooth surface. Dental enamel formation begins during the second trimester of pregnancy and is complete by about 18 years of age.[6] The major portion of the newborn's stores of calcium and phosphorus are accumulated in the third trimester of pregnancy. Therefore, an ELBW infant will not have accumulated these stores. Enamel hypoplasia is defined as "deficient quantity of enamel resulting from developmental aberrations, and may occur in the form of pits, grooves, or larger areas of missing enamel."[6] Enamel opacity is defined as a qualitative change in the translucency of the enamel.[7]

The common medical complications of premature infants including surfactant-deficiency respiratory distress syndrome, asphyxia and hypoxia, hypocalcemia, renal immaturity, feeding difficulties, and infection are just some of the problems that may affect enamel formation. The biochemical cause of enamel hypoplasia is not fully understood, but growing evidence indicates it is strongly linked to calcium homeostasis.[1] There are several studies that suggest a direct relationship between enamel hypoplasia in primary teeth and neonatal hypocalcemia.[2,8] There are numerous pre- and postnatal problems that cause hypocalcemia in the newborn. The more premature and the lower the birth weight, the more problems with calcium homeostasis. Maternal diabetes mellitus, placental insufficiency, often related to preeclampsia, and maternal deficiency of dietary calcium and vitamin D are all in utero factors. Traumatic delivery, asphyxia, cerebral injury, and prematurity itself with deranged calcium metabolism are perinatal factors that contribute to hypocalcemia. Additional contributors to hypocalcemia include hypoxia, sepsis, and hyperbilirubinemia.

The prevalence of enamel defects ranges from 43% to 96% of VLBW infants.[9,10,11] Seow et al reported a direct relationship between birth weight and gestational age with the greatest prevalence of enamel defects occurring in the lowest birth weight group.[9] The clinical significance of enamel defects is not only esthetic, although these teeth can appear cream colored, yellow, or brown. Enamel hypoplasia is linked to plaque accumulation, dental caries, and in more severe cases, with space loss and malocclusion. In a longitudinal study by Lai et al[5] there was a significant association with enamel defects and dental caries in the VLBW group that was noted on exams of the children at 44 and 52 months of age. The most dental caries were observed in those children who had both enamel hypoplasia and opacity.

Enamel defects have also been identified in the permanent dentition of children born prematurely. Pimlott et al[4] found enamel hypocalcification in at least one maxillary permanent incisor in 58% of the 106 VLBW infants examined; however, the other permanent teeth were not examined. Seow[12] matched 55 VLBW and 55 normal birth weight (NBW) controls at a mean age of 7.7 years for defects in enamel of permanent incisors and molars. The VLBW group had a higher percentage of enamel defects in the permanent molars (21% v 11%) and permanent lateral incisors (12% v 0%) compared with controls. Most of the defects were enamel opacities. Aine et al[13] matched 32 preterm to 64 control children. The prevalence of enamel defects in preterm compared with control children was higher in both primary (78% v 20%) and permanent (83% v 36%) dentitions. Because the permanent teeth are believed to begin mineralization a few months after the preterm birth, it is hypothesized that persistent metabolic disturbances affect the mineralization and calcium homeostasis of the first few permanent teeth.

Enamel defects can be both generalized or localized. Generalized defects are symmetrically distributed and likely caused by systemic illnesses associated with prematurity. As mineral stores in the preterm infant are depleted, calcium and phosphorus entering the developing tooth is insufficient for enamel formation. This theory is supported by a study of preterm children who had neonatal rickets secondary to severe osteopenia.[9] In the study, every child with rickets also had severe enamel hypoplasia. A later study by the same investigators[14] demonstrated that all preterm children with enamel hypoplasia also had decreased cortical mineralization of the humerus. This study demonstrated a direct relationship between enamel hypoplasia and diminished bone mineral stores.

Trauma may also cause some enamel defects. Controlled studies by Seow et al[9,14] demonstrated that children who had been orally intubated and required mechanical ventilation had more enamel defects on the left maxillary teeth (63% v 40%) compared with nonintubated children. A Swedish study[15] of full-term infants who were intubated in the neonatal period demonstrated similar results of more defects on the left side. The process of laryngoscopy would account for this primarily left side defect. Inadvertent force is often placed on the left side as the laryngoscope is pushed more to that side to allow room to insert the orotracheal tube along a groove in the right side. Although the tube itself has been considered to be the cause of the trauma, the tube would likely cause more even distribution of force to both right and left sides.

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