Initiation

The primary teeth form in dental crypts that arise from a band of epithelial cells incorporated into each developing jaw. By 12 wk of fetal life, each of these epithelial bands (dental laminae) has 5 areas of rapid growth on each side of the maxilla and the mandible, seen as rounded, budlike enlargements. Organization of adjacent mesenchyme takes place in each area of epithelial growth, and the 2 elements together are the beginning of a tooth.

After the formation of these crypts for the 20 primary teeth, another generation of tooth buds forms lingually (toward the tongue), which will develop into the succeeding permanent incisors, canines, and premolars that eventually replace the primary teeth. This process takes place from ∼5 mo of gestation for the central incisors to ~10 mo of age for the 2nd premolars. The permanent 1st, 2nd, and 3rd molars, on the other hand, arise from extension of the dental laminae distal to the 2nd primary molars; buds for these teeth develop at ∼4 mo of gestation, 1 yr of age, and 4-5 yr of age, respectively.

Histodifferentiation-Morphodifferentiation

As the epithelial bud proliferates, the deeper surface invaginates and a mass of mesenchyme becomes partially enclosed. The epithelial cells differentiate into the ameloblasts that lay down an organic matrix that forms enamel; the mesenchyme forms the dentin and dental pulp.

Calcification

After the organic matrix has been laid down, the deposition of the inorganic mineral crystals takes place from several sites of calcification that later coalesce. The characteristics of the inorganic portions of a tooth can be altered by disturbances in formation of the matrix, decreased availability of minerals, or the incorporation of foreign materials. Such disturbances can affect the color, texture, or thickness of the tooth surface. Calcification of primary teeth begins at 3-4 mo in utero and concludes postnatally at ∼12 mo with mineralization of the 2nd primary molars (Table 299-1).

Eruption

At the time of tooth bud formation, each tooth begins a continuous movement toward the oral cavity. The times of eruption of the primary and permanent teeth are listed in Table 299-1.

Anomalies Associated with Tooth Development

Both failures and excesses of tooth initiation are observed. Developmentally missing teeth can result from environmental insult, a genetic defect involving only teeth, or the manifestation of a syndrome. Anodontia, or absence of teeth, occurs when no tooth buds form (ectodermal dysplasia, or familial missing teeth) or when there is a disturbance of a normal site of initiation (the area of a palatal cleft). The teeth that are most commonly absent include the 3rd molars, the maxillary lateral incisors, and the mandibular 2nd premolars.

If the dental lamina produces more than the normal number of buds, supernumerary teeth occur, most often in the area between the maxillary central incisors. Because they tend to disrupt the position and eruption of the adjacent normal teeth, their identification by radiographic examination is important. Supernumerary teeth also occur with cleidocranial dysplasia (Chapter 303) and in the area of cleft palates.

Twinning, in which 2 teeth are joined together, is most often observed in the mandibular incisors of the primary dentition. It can result from gemination, fusion, or concrescence. Gemination is the result of the division of 1 tooth germ to form a bifid crown on a single root with a common pulp canal; an extra tooth appears to be present in the dental arch. Fusion is the joining of incompletely developed teeth that, owing to pressure, trauma, or crowding, continue to develop as 1 tooth. Fused teeth are sometimes joined along their entire length; in other cases, a single wide crown is supported on 2 roots. Concrescence is the attachment of the roots of closely approximated adjacent teeth by an excessive deposit of cementum. This type of twinning, unlike the others, is found most often in the maxillary molar region.

Disturbances during differentiation can result in alterations in dental morphology, such as macrodontia (large teeth) or microdontia (small teeth). The maxillary lateral incisors can assume a slender, tapering shape (peg-shaped laterals).

Amelogenesis imperfecta represents a group of hereditary conditions that manifest in enamel defects of the primary and permanent teeth without evidence of systemic disorders (Fig. 299-1). The teeth are covered by only a thin layer of abnormally formed enamel through which the yellow underlying dentin is seen. The primary teeth are generally affected more than the permanent teeth. Susceptibility to caries is low, but the enamel is subject to destruction from abrasion. Complete coverage of the crown may be indicated for dentin protection, to reduce tooth sensitivity, and for improved appearance.

Figure 299-1 Amelogenesis imperfecta, hypoplastic type. The enamel defect results in areas of missing or thin enamel as well as grooves and pits.

Dentinogenesis imperfecta, or hereditary opalescent dentin, is a condition analogous to amelogenesis imperfecta in which the odontoblasts fail to differentiate normally, resulting in poorly calcified dentin (Fig. 299-2). This autosomal dominant disorder can also occur in patients with osteogenesis imperfecta. The enamel-dentin junction is altered, causing enamel to break away. The exposed dentin is then susceptible to abrasion, in some cases worn to the gingiva. The teeth are opaque and pearly, and the pulp chambers are generally obliterated by calcification. Both primary and permanent teeth are usually involved. If there is excessive wear of the teeth, selected complete coverage of the teeth may be indicated to prevent further tooth loss and improve appearance.

Figure 299-2 Dentinogenesis imperfecta. The bluish, opalescent sheen on several of these teeth results from genetically defective dentin. This condition may be associated with osteogenesis imperfecta.

(From Nazif MM, Martin BS, McKibben DH, et al: Oral disorders. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, ed 4, Philadelphia, 2002, Mosby, p 703.)

Localized disturbances of calcification that correlate with periods of illness, malnutrition, premature birth, or birth trauma are common. Hypocalcification appears as opaque white patches or horizontal lines on the tooth; hypoplasia is more severe and manifests as pitting or areas devoid of enamel. Systemic conditions, such as renal failure and cystic fibrosis, are associated with enamel defects. Local trauma to the primary incisors can also affect calcification of permanent incisors.

Fluorosis (mottled enamel) can result from systemic fluoride consumption >0.05 mg/kg/day during enamel formation. This high fluoride consumption can be caused by residing in an area of high fluoride content of the drinking water (>2.0 ppm), swallowing excessive fluoridated toothpaste, or inappropriate fluoride prescriptions. Excessive fluoride during enamel formation affects ameloblastic function, resulting in inconspicuous white, lacy patches on the enamel to severe brownish discoloration and hypoplasia. The latter changes are usually seen with fluoride concentrations in the drinking water >5.0 ppm.

Discolored teeth can result from incorporation of foreign substances into developing enamel. Neonatal hyperbilirubinemia can produce blue to black discoloration of the primary teeth. Porphyria produces a red-brown discoloration. Tetracyclines are extensively incorporated into bones and teeth and, if administered during the period of formation of enamel, can result in brown-yellow discoloration and hypoplasia of the enamel. Such teeth fluoresce under ultraviolet light. The period at risk extends from ∼4 mo of gestation to 7 yr of life. Repeated or prolonged therapy with tetracycline carries the highest risk.

Delayed eruption of the 20 primary teeth can be familial or indicate systemic or nutritional disturbances such as hypopituitarism, hypothyroidism, cleidocranial dysplasia, trisomy 21, and multiple syndromes. Failure of eruption of single or small groups of teeth can arise from local causes such as malpositioned teeth, supernumerary teeth, cysts, or retained primary teeth. Premature loss of primary teeth is most commonly caused by premature eruption of the permanent teeth. If the entire dentition is advanced for age and sex, precocious puberty or hyperthyroidism should be considered.

Natal teeth are observed in ∼1/2,000 newborn infants; usually, there are 2 in the position of the mandibular central incisors. Natal teeth are present at birth, whereas neonatal teeth erupt in the 1st mo of life. Attachment of natal and neonatal teeth is generally limited to the gingival margin, with little root formation or bony support. They may be a supernumerary or a prematurely erupted primary tooth. A radiograph can easily differentiate between the 2 conditions. Natal teeth are associated with cleft palate, Pierre Robin syndrome, Ellis-van Creveld syndrome, Hallermann-Streiff syndrome, pachyonychia congenita, and other anomalies. A family history of natal teeth or premature eruption is present in 15-20% of affected children.

Natal or neonatal teeth occasionally result in pain and refusal to feed and can produce maternal discomfort because of abrasion or biting of the nipple during nursing. If the tooth is mobile there is a danger of detachment, with aspiration of the tooth. Because the tongue lies between the alveolar processes during birth, it can become lacerated, and, occasionally, the tip is amputated (Riga-Fede disease). Decisions regarding extraction of prematurely erupted primary teeth must be made on an individual basis.

Exfoliation failure occurs when a primary tooth is not shed before the eruption of its permanent successor. Most often the primary tooth exfoliates eventually, but in some cases, the primary tooth needs to be extracted. This occurs most commonly in the mandibular incisor region.