Mechanism And Timing Of Fluoride Effects On Developing Enamel Pdf

mechanism and timing of fluoride effects on developing enamel pdf

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Enamel formation is initiated in a neutral pH environment secretory stage ; however, the pH can fall to below 6.

Oper Dent 1 November ; 44 6 : — The present clinical case report describes the clinical steps of enamel microabrasion associated with dental bleaching to restore severely-pitted fluorosed teeth. The process of removing the fluorotic superficial stains started by using macroabrasion with a water-cooled fine tapered FF diamond bur. Rubber dam isolation of the operative field was used to remove the remaining enamel stains and superficial irregularities with the Opalustre microabrasive compound 6.

Alimentary fluoride intake in preschool children

Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Review Free to read. Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure as it relates to dental fluorosis occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2—3 years of age, and end after mineralization of the third molars.

The white opaque appearance of fluorosed enamel is caused by a hypomineralized enamel subsurface; with more severe dental fluorosis, pitting and a loss of the enamel surface occurs, leading to secondary staining appearing as a brown color. At the early maturation stage, the relative quantity of amelogenin protein is increased in fluorosed enamel in a dose-related manner.

This appears to result from a delay in the removal of amelogenins as the enamel matures. In vitro, when fluoride is incorporated into the mineral, more protein binds to the forming mineral, and protein removal by proteinases is delayed.

Fluoride also appears to enhance mineral precipitation in forming teeth, resulting in hypermineralized bands of enamel, which are then followed by hypomineralized bands.

Enhanced mineral precipitation with local increases in matrix acidity may affect maturation stage ameloblast modulation, potentially explaining the doserelated decrease in cycles of ameloblast modulation from ruffleended to smooth-ended cells that occur with fluoride exposure in rodents.

Specific cellular effects of fluoride have been implicated, but more research is needed to determine which of these changes are relevant to the formation of fluorosed teeth.

As further studies are done, we will better understand the mechanisms responsible for dental fluorosis. Excess fluoride ingestion results in dental fluorosis. The mechanisms affected by longterm chronic exposure to low levels of fluoride are likely to differ from those affected by acute exposures to high levels of fluoride [ 1 — 3 ]. Some mechanisms affected by lower chronic fluoride levels, resulting in enamel fluorosis, are likely to be specific to this uniquely mineralizing tissue, while others may also affect other cells and tissues.

Enamel fluorosis refers to fluoride-related al-terations in enamel, which occur duringenamel development. These alterations become more severe with increasing fluoride intake, and time of exposure. The severity of fluorosis is related to the concentration of fluoride in the plasma, considered to be in equilibrium with the tissue fluid that bathes the enamel organ [ 4 , 5 ]. Plasma fluoride levels are influenced by many factors, including total fluoride intake, type of intake i.

In addition to these variables, genetic factors have been shown to dictate the severity of enamel fluorosis in mice [ 7 ]. A complicating factor in assessing the exact dose, or determining the stages of enamel formation most sensitive to fluoride, is that fluoride incorporated into bone is gradually released by continuous bone remodeling [ 5 , 8 ].

Levels of plasma fluoride as low as 1. The effects of chronic fluoride exposure have also been linked to effects on other tissues and systems [ 9 ]. However, in this chapter, we will focus primarily on the effects of fluoride on tooth development. The largest body of research has investigated the effects of fluoride on enamel formation, with much less known about the potential effects of fluoride on dentin formation.

Therefore, most of the focus will be on enamel fluorosis. The sections of this chapter comprise:. Clinically, mild cases of dental fluorosis are characterized by a white opaque appearance of the enamel, caused by increased subsurface porosity fig. The earliest sign is a change in color, showing many thin white horizontal lines running across the surfaces of the teeth, with white opacities at the newly erupted incisal end. Dental fluorosis. At higher levels of fluoride exposure, the white lines in the enamel become more and more defined and thicker.

Some patchy cloudy areas and thick opaque bands also appear on the involved teeth. With increased dental fluorosis, the entire tooth can be chalky white and lose transparency [ 10 , 12 ]. With higher fluoride doses or prolonged exposure, deeper layers of enamel are affected; the enamel becomes less well mineralized. Damage to the enamel surface occurs in patients with moderate-to-severe degrees of enamel fluorosis. Teeth can erupt with pits, with additional pitting occurring with posteruptive enamel fracture.

In the individuals with moderate dental fluorosis, yellow to light brown staining is observed in the areas of enamel damage. In very severe cases, the enamel is porous, poorly mineralized, stains brown, and contains relatively less mineral and more proteins than sound enamel. Severely fluorosed enamel can easily chip posteruptively during normal mechanical use [ 13 , 14 ]. Although teeth with mild dental fluorosis may be more resistant to dental decay because of the higher levels of fluoride contained in the enamel surface, severely fluorosed teeth are more susceptible to decay, most likely because of the uneven surface or loss of the outer protective layer [ 15 ].

In , H. Dean developed an index to describe and diagnosis enamel fluorosis [ 16 , 17 ]. He scored the fluorotic teeth into 6 categories according to their clinical manifestations, including normal teeth, which were given a score of 0 table 1.

The treatments for fluorotic teeth are limited. For the mildest forms of fluorosis TFI 1, 2 bleaching can be recommended. Treatments for moderate dental fluorosis include microabrasion, where the outer affected layer of enamel is abraded from the tooth surface in an acidic environment. Specific guidelines for different ages table 2 were published by the US Food and Nutrition Board of the Institute of Medicine in , recommending total daily fluoride intakes [ 21 ].

In this guideline, the suggested total daily exposure dosage for infants younger than 6 months of age of 0. These guidelines suggest greater attention should be given to the total fluoride intake of infants from water used to dilute infant formulas, foods and other supplement sources. US National Academy of Sciences. Institute of Medicine. Food and Nutrition Board. There are multiple sources of fluoride and all have the potential to cause dental fluorosis — including natural fluoride, artificial or added fluoride in drinking water and dental products, as well as occupation-related exposures.

Dental fluorosis resulting from high fluoride levels in underground water is an issue in specific regions of the world. Fluoride can exist in an ionized form in ground waters, and in areas where the soil lacks calcium — such as occurs in areas with high levels of granite or gneiss — relatively high fluoride levels are detected in groundwater.

When the level of fluoride is above 1. In some parts of Africa, China, the Middle East and southern Asia India, Sri Lanka , as well as some areas in the Americas and Japan, high concentrations of ionic fluoride have been found in ground waters, vegetables, fruit, tea and other crops, although drinking water is usually the major source of the daily fluoride intake [ 22 ].

The atmosphere in these areas may have high levels of fluoride from dust in areas with fluoride-containing soils and gas, released from industries, underground coal fires and volcanic activities [ 22 ].

In the USA, approximately 10 million people are exposed to naturally fluoridated public water. In , it was reported that 6. Some areas have extremely high concentrations of fluoride in drinking water — such as in Colorado Two primary sources have been identified as being potentially responsible for the prevalence of dental fluorosis: fluoride in drinking water and fluoride-containing dental products including fluoride supplements.

Since , fluoride has been used as a supplement in many public drinking water systems to control dental decay [ 23 ]. In , approximately million people The level of fluoridation is lower in high-temperature areas as people usually drink more water. The fluoridation of public drinking water has significantly decreased the incidence of dental decay at a relatively low cost.

In the studies by Dean and colleagues completed in the s, the risk of dental fluorosis at 1 ppm fluoride in drinking water was extremely low, particularly in relation to the impact of fluoride on dental caries fig.

Following these studies, water fluoridation was considered by the US Centers for Disease Control to be 1 of the 10 great public health achievements in the 20th century [ 25 ]. Concentrations of fluoride in drinking water are related to caries incidence in children and severity of dental fluorosis. However, as fluoride has become more widely used in dental products toothpastes, mouth rinses, fluoride supplements and been incorporated into food sources via fluoridated water , multiple sources of fluoride exposure are now related to the reported increase in the incidence of dental fluorosis.

In the USA, the prevalence of dental fluorosis appears to be increasing. Change in dental fluorosis prevalence among children aged 12—15 years participating in 2 national surveys in the USA — and — Percentages do not sum to due to rounding. School Children — [ 27 ]. The incidence of very mild and greater fluorosis in persons aged 6—39 years was The increased prevalence of fluorosis in black non-Hispanics may suggest a genetic influence on fluorosis susceptibility. All estimates are adjusted by age single years and sex to the USA standard population, except sex, which is adjusted only by age.

The primary pathological finding of fluorosed enamel is a subsurface porosity, along with hyper and hypomineralized bands within the forming enamel fig. Fluoride can also result in mineralization-related effects on dentin formation. Microradiograph of fluorosed enamel from Colorado Springs.

Note the radiolucent outer third of the enamel with a well-calcified surface layer. From Newbrun [ 97 ], reprinted with permission. Severely fluorosed human dentin is characterized by a highly mineralized sclerotic background pattern, scattered with hypomineralized porous lesions primarily in the subsurface area.

Scanning electron microscope images show dentin tubules with an irregular distribution and narrow and disrupted lumina, rather than the regular appearing lumina seen in normal dentin [ 35 ].

The pathogenesis of dental fluorosis is related to physiological conditions, including body weight, rate of skeletal growth and remodeling, nutrition, and renal function [ 36 — 38 ]. Bone is a reservoir of fluoride, as fluoride is incorporated in the forming apatite crystals, and this ion can also be released from these crystals as bone remodels. Therefore, rapid bone growth, as occurs in the growing child, will remove fluoride from the blood stream, possibly reducing the risk of dental fluorosis by lowering serum fluoride levels [ 8 , 39 ].

Nutrition is also important for controlling the serum level of fluoride, as ions such as calcium, magnesium and aluminum can reduce the bioavailability of fluoride. A deficiency in these ions in food can also affect enhance fluoride up take [ 40 ]. Genetic background appears to have role in the pathogenesis of dental fluorosis. This may be the reason why in human populations, individuals drinking water with similar fluoride contents have a wide range of severity of dental fluorosis fig.

Evidence for a genetic component to fluoride susceptibility comes from work by Everett et al. They concluded that there is a genetic component to dental fluorosis susceptibility [ 41 , 42 ].

Fluoride is a single highly electronegative ion that interacts with the cells and matrix at the different stages of enamel formation in relation to fluoride dose and time of exposure. Tooth enamel development can be divided into 4 major stages: pre-secretory, secretory, transition and maturation stages, all with unique properties that affect fluoride susceptibility.

Most of the studies of the mechanisms of fluoride in forming fluorosed enamel have used the rodent incisor or molars as a model, as it is not possible to do similar studies using human teeth. The rodent incisor is a continuously erupting tooth, with all stages of enamel formation present in each tooth, whereas the molar is a rooted tooth, which begins formation in utero.

Difficulties in identifying developmental defects of the enamel: a BITA study

Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Review Free to read. Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure as it relates to dental fluorosis occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2—3 years of age, and end after mineralization of the third molars.

Metrics details. The knowledge of background alimentary fluoride intake in preschool children is of utmost importance for introducing optimal and safe caries preventive measures for both individuals and communities. The aim of this study was to assess the daily fluoride intake analyzing duplicate samples of food and beverages. An attempt was made to calculate the daily intake of fluoride from food and swallowed toothpaste. Daily alimentary fluoride intake was measured in a group of 36 children with an average age of 4. This was repeated after six months.

Dental caries is still one of the major public health problems. The most effective way of caries prevention is the use of fluoride. The aim of our research was to review the literature about fluoride toxicity and to inform physicians, dentists and public health specialists whether fluoride use is expedient and safe. Data we used in our review were systematically searched and collected from web pages and documents published from different international institutions. Fluoride occurs naturally in our environment but we consume it in small amounts.


Aims: To observe and characterize the histological features of fluorosed teeth under light and confocal microscope CFM. Materials and Methods: A total of 25 fluorosed teeth and 5 normal teeth were collected from dentists across Dindigul, a known endemic area of fluorosis in South India. Ground sections of respective teeth were observed under light microscope and the sections were subsequently stained with acridine orange and studied under CFM.

To evaluate the ability to recognise different types of developmental defects of enamel DDE by a group of general dental staff, trained prior to the comprehensive prevalence study the BITA study , and to compare their skills to that of an untrained group. To evaluate the reliability of an MIH diagnose, 3 years after the study ended. A test protocol with 24 digital photos of teeth with different DDE was filled out. Ninety-one patients with reported DDE were clinically re-examined 3 years later by two dentists with certified experience of DDE.

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