Deciduous enamel defects in low-birth-weight children: correlated X-ray microtomographic and backscattered electron imaging study of hypoplasia and hypomineralization.

Enamel does not remodel, and disturbances occurring during development may remain in the tooth as a permanent record of the upset. Mineralization in prenatal and postnatal deciduous enamel was studied in the shed deciduous incisors of low-birth-weight (LBW: < 2kg) children. The specific objective was to gain further insight into the mechanism of formation of developmental defects of enamel. Sections at a resolution of 22-40 microns were reconstructed using X-ray microtomography (microCT) giving absolute measurements of linear absorption coefficient for AgK alpha radiation. Detail to ca. 1 micron resolution was obtained using automated, digital backscattered electron (BSE) imaging of PMMA-embedded material. Matching the histograms of BSE and microCT images made possible the calibration of the mean atomic number-dependent signal in the BSE images. The comparison of abnormal, affected enamel regions and post-recovery, normal, unaffected regions could be made in the same teeth, since these zones were easily recognized from the distribution of hypoplasia and hypomineralization. The microCT values, converted to calculated mineral densities, ranged from 2.3 g cm-3 to 2.6 g cm-3 in LBW hypoplastic, and between 2.65 and 2.78 g cm-3 in control primary enamel and post-defect, post-natal LBW enamel. Hypoplasia with or without minimal hypomineralization indicated recovery of the ameloblasts in the maturation phase. Disturbance during late matrix formation and early maturation resulted in hypoplasia and hypomineralization.