Developmental anomalies of teeth are marked deviations from the normal standards in color, contour, size, number, and degree of development of the teeth. Systemic as well as local factors may operate to produce these developmental disturbances. Such influences may begin before or after birth so that either deciduous or permanent teeth may be involved. Usually, it is the permanent teeth that are influenced and, in all instances, only those not completely formed at the time of the disturbance.
2-14. HYPOPLASIA (Figure 2-14)
In hypoplasia, there is a lack of development or a defective development of the enamel of the tooth before its eruption. In deciduous teeth, enamel hypoplasia can be caused by a disturbance in the enamel formation before birth and, for some deciduous teeth, after birth. In permanent teeth, enamel hypoplasia can only be caused by some disturbance after birth since enamel formation of the permanent dentition begins at
birth. Enamel prisms are deposited by the enamel organ in a definite pattern to form the crown of the tooth. A local disturbance may interfere with this process and result in defective development. The degree of the defect (hypoplasia) varies from mild, shallow depressions or grooves to extensive grooves or pits arranged in horizontal rows around the crown. These grooves or pits extend into the enamel as far as the dentinoenamel junction. The defect may be a lack of development of all or part of the enamel, leaving exposed dentin. Hypoplastic enamel and poorly formed dentin can be attributed to various causes or combinations of causes, such as infectious diseases (scarlet fever, measles, pneumonia), rickets, or hereditary factors. Trauma to primary teeth may cause a localized hypoplastic defect in a developing permanent tooth (called Turner's tooth). Prevention is much better than treatment. A physician who provides good health supervision (including proper treatment of infant disease) and good nutrition are the keys to prevention.
Anodontia, which means absence of teeth, is an anomaly in which the enamel organ fails to form. Some (partial anodontia) or all (total anodontia) of the teeth may fail to develop. Cases in which only part of the tooth fails to form are considered forms of hypoplasia.
2-16. ENAMEL HYPOCALCIFICATION
Defective development of the enamel matrix may cause hypocalcification. This implies a poor quality of enamel although the amount is normal. The enamel may be chalky, crumble easily, and contain white or brown areas or spots. Dental fluorosis is a form of hypocalcification.
2-17. MOTTLED ENAMEL (Figure 2-15)
Mottled enamel, or dental fluorosis, is a form of enamel hypocalcification which results from the ingestion of excessive fluoride during the period of enamel formation. To cause mottling, fluoride must be present in concentrations several times that found in controlled fluoridated water supplies. The mottling of enamel varies in extent and severity, depending on the amount of fluoride in the water and how long it was routinely used. In mild cases, the enamel is opaque but of good structure. In severe cases, it may be chalky and crumble easily. The area of involvement varies from spots on a few teeth to extensive mottling of many teeth. The mottled areas may have a white, opaque appearance or they may have a stained appearance ranging from yellowish-brown to dark-brown. This condition is significant because it makes teeth unsightly. Superficial bleaching and acid etch composite may be used to correct the condition. Severe cases may require porcelain veneers or crowns.
2-18. SUPERNUMERARY TEETH (Figures 2-16 and 2-17)
Dental hyperplasia may result in additional enamel organs being formed, resulting in development of teeth beyond the normal number (32 permanent teeth). Hyperplasia is defined as an increase in the number of individual tissue elements. This may also account for supernumerary cusps or roots within the normal complement of teeth; see figure 2-16. The vast majority of supernumerary teeth occur in the maxilla, with the most common being a mesiodens (a tooth located between the permanent maxillary central incisors); see figure 2-17.
2-19. OTHER DEVELOPMENTAL ANOMALIES
|David L. Heiserman, Editor||
Copyright © SweetHaven
Revised: June 06, 2015