Abstract
The literature on tooth formation in children with cleft lip and/or palate is reviewed. The main focus of interest is the association of cleft type and dental abnormalities in number, size, shape, timing of formation, and eruption and cause of the abnormalities. The upper lateral incisor is the most susceptible to injury in the area of cleft in both deciduous and permanent dentitions. This tooth is affected in most instances, even in the cases of microforms of the cleft lip. The prevalence of hypodontia increases strongly with the severity of cleft. More teeth are congenitally missing from the upper jaw than from the lower jaw; however, in the permanent dentition both jaws are affected. Very high prevalence of hypodontia are observed in connection with the Van der Woude syndrome associated with cleft and with the Pierre Robin anomaly. Hypodontia is similarly prevalent in subjects with isolated cleft palate with and without a positive family history of clefts. The prevalence of hypodontia varies largely in different populations. Asymmetric formation of the contralateral teeth is a milder form of hypodontia. The prevalence of asymmetrically developing pairs of teeth is far more common in children with clefts than in children with normal palates or lips. In the permanent dentition the timing of tooth formation is delayed in children from all cleft groups compared to noncleft children. The delay lengthens (with increasing severity of cleft) from 0.3 to 0.7 years and is similar in all permanent teeth in both jaws. In children with hypodontia, the delay is still more severe. As the child becomes older, the delay may increase. The size of the permanent teeth is smaller than in noncleft children and the metric asymmetry of the crown or root size is apparent in both jaws. Enamel defects and abnormalities in shape and size of both deciduous and permanent teeth are far more common in children and fetuses affected with cleft than in normal subjects. These abnormalities occur in both jaws. Dental abnormalities in number, size, shape, timing of formation, eruption, and the cleft itself seem to have a common cause in most instances. The postnatal environmental factors-nutrition, infections, and surgical treatment—may have an effect only on enamel defects and, perhaps, in some instances, on agenesis of the permanent teeth.
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