Developmental defects of enamel are visible deviations from the normal translucent appearance of tooth enamel resulting from enamel organ dysfunction. In the past, information about the activities of the ameloblasts has determined the terminology used to describe the lesions. Advances in our understanding of the complicated secretory and maturation phases of amelogenesis have required a re-appraisal of the concepts of defect formation. The phase of ameloblast activity, the duration of the disturbance, and its severity leading to temporary or permanent inactivity of the cells determine the appearance of the three common types of lesions--hypoplasia, and diffuse and demarcated opacities.

Over 1000 children, participating in a longitudinal study of health and development, possess documented medical histories based on birth records and regular assessments starting at age 3. A dental examination at age 5 of 923 participants recorded their exposure to fluoride and evidence of trauma to the deciduous teeth. The prevalence of developmental defects of dental enamel in 696 of the children when aged 9 was reported as 56% (Suckling et al., 1985). For the present study, a number of illnesses, accidents, and other experiences were selected from the recorded information as possible etiological factors for any defect, demarcated and diffuse opacities, and hypoplasia. Despite extensive statistical testing, positive and strong associations were few. The prevalence of hypoplasia, seen in 15% of the sample, was higher in those children who had chicken pox before age 3 and, as reported previously, in those children with a history of trauma to their deciduous incisors. This study illustrates the difficulty of establishing the etiology of enamel defects, even when medical and dental histories are available.

Defects present in 12 human permanent teeth were classified on the basis of their macroscopic appearance as hypoplasia (three teeth), diffuse opacities (three teeth), white demarcated opacities (one tooth but two defects), or yellow demarcated opacities (five teeth but six defects). The hardness values and SEM appearance of the defective enamel were determined after the teeth were sectioned through the lesion(s) and were distinctive for each type of defect. The thin enamel of the hypoplastic lesions was either opaque (with reduced hardness values) or translucent (with near-normal hardness values and sometimes a change in prism orientation external to an incremental line). The enamel of the diffuse and demarcated opacities was of normal thickness. The changes in the macroscopic and SEM appearance, and the reduced hardness values of the diffuse patchy opacities, were restricted to the outer 150 microns of the enamel. The demarcated opacities varied in position and depth, and in places had a clearly marked boundary with the adjacent normal enamel. Hardness values were related to color change, with yellow lesions being softer than white. Although prism direction was normal within demarcated opacities, prism outlines were less distinct. The findings suggest that temporary and permanent dysfunction of ameloblasts can occur in both secretory and maturation phases, influencing the final appearance of the lesion.

The prevalence of developmental defects of enamel was assessed in 243 children aged 12-14 yr using the FDI Index. The teeth were not cleaned or dried prior to examination for which fibre optic lighting was used. At least one tooth with defective enamel was seen in 63% of children with a demarcated white opacity present in 44% of children. The enamel was abnormal in 11.7% of teeth, diffuse patchy opacities and demarcated white opacities occurring in 4.4 and 4.2%, respectively. Although defects were found most frequently in the maxillary central incisors, the ranking order of prevalence and the distribution for demarcated and diffuse opacities was quite different. Sex, residence, and the common childhood illnesses did not alter the prevalence of defects which was, however, increased significantly in 22 children with a history of a serious illness or accident (0.01 greater than P greater than 0.001). The prevalence of the diffuse opacities was significantly increased with increased exposure to fluoride either in tablets or in the drinking water (0.01 greater than P greater than 0.001).

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