Clinical and Histological Features

Enamel fluorosis is a mottling of the tooth surface that is attributed to fluoride exposure during tooth formation. The process of enamel maturation consists of an increase in mineralization within the developing tooth and concurrent loss of early-secreted matrix proteins. Exposure to fluoride during maturation causes a dose-related disruption of enamel mineralization resulting in widening gaps in its crystalline structure, excessive retention of enamel proteins, and increased porosity. These effects are thought to be due to fluoride’s effect on the breakdown rates of matrix proteins and on the rate at which the by-products from that degradation are withdrawn from the maturing enamel (Aoba and Fejerskov 2002).

Clinically, mild forms of enamel fluorosis are evidenced by white horizontal striations on the tooth surface or opaque patches, usually located on the incisal edges of anterior teeth or cusp tips of posterior teeth. Opaque areas are visible in tangential reflected light but not in normal light. These lesions appear histopathologically as hypomineralization of the subsurface covered by a well-mineralized outer enamel surface (Thylstrup and Fejerskov 1978). In mild fluorosis, the enamel is usually smooth to the point of an explorer, but not in moderate and severe cases of the condition (Newbrun 1986). In moderate to severe forms of fluorosis, porosity increases and lesions extend toward the inner enamel. After the tooth erupts, its porous areas may flake off, leaving enamel defects where debris and bacteria can be trapped. The opaque areas can become stained yellow to brown, with more severe structural damage possible, primarily in the form of pitting of the tooth surface.

Enamel in the transitional or early maturation stage of development is the most susceptible to fluorosis (DenBesten and Thariani 1992). For most children, the first 6 to 8 years of life appear to be the critical period of risk. In the Ikeno district of Japan, where a water supply containing fluoride at 7.8 mg/L was inadvertently used for 12 years, no enamel fluorosis was seen in any child who was age 7 years or older at the start of this period or younger than 11 months old at the end of it (Ishii and Suckling 1991). For anterior teeth, which are of the most aesthetic concern, the risk period appears to be the first 3 years of life (Evans and Stamm 1991; Ishii and Suckling 1991; Levy et al. 2002a). Although it is possible for enamel fluorosis to occur when teeth are exposed during enamel maturation alone, it is unclear whether it will occur if fluoride exposure takes place only at the stage of enamel-matrix secretion. Fejerskov et al. (1994) noted that fluoride uptake into mature enamel is possible only as a result of concomitant enamel dissolution, such as caries development. Because the severity of fluorosis is related to the duration, timing, and dose of fluoride intake, cumulative exposure during the entire maturation stage, not merely during critical periods of certain types

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