Dental fluorosis (also called marottel buxel ) is a very common disorder, characterized by tooth enamel hypogineralization caused by excessive fluoride consumption during enamel formation.
It appears as a variety of visual changes in the enamel that cause the degree of discoloration of the intrinsic tooth, and, in some cases, physical damage to the teeth. The severity of the condition depends on the dose, duration, and age of the individual during the exposure. The "very light" (and most common) form of fluorosis, is characterized by a small, opaque white "paper" area spread over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these crooked spots may involve up to half of the surface area of ​​the tooth. When fluorosis is moderate, all surfaces of teeth are streaked and teeth may be grounded and brown stains often "damage" teeth. Severe fluorosis is characterized by discoloration of brown and discrete or confluent pitting; brown stains are widespread and teeth often show a rusty appearance.
People with fluorosis are relatively resistant to dental caries (tooth decay caused by bacteria), although they may have cosmetic problems. In moderate to severe fluorosis, the tooth is physically damaged.
Video Dental fluorosis
Diagnosis
Adequate fluorosis diagnosis can be diagnosed by visual clinical examination. This requires examination of the surface of dry and clean teeth under good lighting. There are individual variations in clinical fluorosis manifestations that are highly dependent on the duration, time, and dose of fluoride exposure. There is a classification difference for diagnosing severity based on appearance. Clinical manifestations of mild tooth fluorosis are largely characterized by the appearance of snowflakes that have no clear boundaries, opaque, white spots, narrow white lines following pericymata or patches because turbidity may coalesce with a solid, hard and smooth enamel surface in large part tooth gear. With increasing severity, subsurface enamel, all the teeth become more porous. The enamel may appear yellow/brown and/or numerous and white-brown spots that look like cavities. They are often described as "spotted teeth". Fluorosis does not cause discoloration of the enamel directly, such as when an eruption into the mouth, the affected permanent tooth does not change color. In tooth enamel, fluorosis causes subsurface subsuries or hypomineralizations, which extend to the dentinal-enamel junction as the severity increases. Therefore, the affected teeth are more susceptible to staining. Due to exogenous ion diffusion (ex, iron and copper), the stain will develop into an abnormally porous enamel.
The differential diagnosis for this condition includes:
- Turner hypoplasia (though this is usually more local)
- Enamel defects caused by undiagnosed and untreated celiac disease.
- Some mild form of amelogenesis imperfecta
- An enamel defect caused by an infection of the primary dental predecessor
- Dental caries: Fluorotic enamel abnormalities are often misdiagnosed as dental caries.
- Dental Trauma: Mechanical trauma to the deciduous tooth can cause a maturation of the maturation phase of enamel formation, which may cause enamel opacity in the permanent successor.
Maps Dental fluorosis
Classification
The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al., 1984), which combines Dean index and TF index; and fluorosis risk index (Pendrys 1990), which is intended to determine the time at which fluoride exposure occurs, and correlates the risk of fluorosis with the stage of dental development.
Dean Index
The Dean fluorosis index was first published in 1934 by H. Trendley Dean. The index undergoes two changes, appearing in the final form in 1942. A person's fluorosis score is based on the heaviest form of fluorosis found in two or more teeth.
TF Index
Proposed by Thylstrup and Fejerskov in 1978, the TF index is a logical extension of the Dean index, combining a modern understanding of the underlying pathology of fluorosis. This spectrum score changes fluorosis in enamel from 0 to 9, allowing a more precise definition of mild and severe cases.
Cause
Dental fluorosis is caused by the amount of fluoride higher than the normal amount when the tooth is formed. Primary fluorine dentin and enamel fluorosis can only occur during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance caused by the surface of the enamel to be hypomineral.
The most superficial concern in dental fluorosis is aesthetic changes in permanent teeth (adult teeth). The period when these teeth are at highest risk of fluorosis is between when a child is born to 6 years of age, although there are some studies that suggest that the most important is during the first 2 years of childhood. From about 7 years after that, most of the children's permanent teeth will have a complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of fluoride intake. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, the individual response, the weight, the level of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.
Many renowned fluoride sources may contribute to overexposure including fluoride mouthwash/mouthwash (which children may ingest), excessive consumption of fluoride toothpaste, bottled water untested for their fluoride content, improper use of fluoride supplements, consumption food is mainly imported from other countries, and fluoridated public water. The latter of these sources is directly or indirectly responsible for 40% of all fluorosis, but the effects resulting from water fluoridation are largely and usually aesthetic. Severe cases can be caused by exposure of naturally fluoridated water to levels above the recommended level, or with exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.
Dental fluorosis has developed in the United States along with fluoridation of urban water supply, albeit disproportionately by race. The CDC 2010 report acknowledged the overall incidence of dental fluorosis 22% from 1986-87 increased to 41% at the beginning of the 21st century, with moderate to severe dental fluorosis upgrading from 1% to 4%. The 2011-12 NHANES figures recorded another 31% increase overall among American teenagers since the previous decade, with a total impact of juvenile population 61% suffering. More than one in five American teenagers (23%) had moderate-to-severe fluorosis in at least two teeth.
Mechanism
Teeth are the most studied body tissue to examine the impact of fluoride on human health. There are several possible mechanisms that have been proposed. It is generally believed that the hypogineralization of affected enamel is primarily due to in-situ toxic effects of fluoride on ameloblasts in enamel formation, and not due to the general effects of fluoride on calcium metabolism, or by the effects of poisoning that suppress fluoride metabolism, however, and decades of research, no research has reinforced the belief mechanism in which dental fluorosis is a result of changes in mineralization that occur when fluroide interacts with tissue mineralization.
In the extra-cellular environment of enamel ripening, the excess fluoride ion changes the rate at which the enamel protein protein (amelogenin) is enzymatically broken down and the rate at which the solvent product is subsequently removed. Fluoride can also indirectly alter protease action through decreasing the availability of free calcium ions in mineralized environments. This results in the formation of enamels with less mineralization. This hypinineral enamel has changed the optical properties and appears opaque and luster relative to the normal enamel.
Traditionally severe fluorosis has been described as enamel hypoplasia, however, hypoplasia does not occur as a result of fluorosis. The holes, ribbons, and loss of enamel regions seen in severe fluorosis are the result of damage to extremely brittle, fragile and fragile enamel messages that occur after they erupt into the mouth.
Hydroxyapatite is converted to fluorohydroxyapatite as follows:
Ca 10 (PO 4 ) 6 (OH) 2 F - - H -> Ca 10 (PO 4 ) 6 (OH) F H 2 O
Manajemen
Teeth fluorosis may or may not be a cosmetic concern. In some cases, there may be different levels of negative psychosocial effects. Treatment options are:
Mild case: Teeth whitening
Medium case: Micro-abrasion (exposed outer layer of enamel rubbed in acid environment)
Serious Case: Composite Patch, Micro-abrasion, Veneer, Crown
Epidemiology
Fluorosis is very common, with 41% of teenagers experiencing definite fluorosis, and another 20% "in doubt" of fluorosis according to the Centers for Disease Control. In 2005 a survey conducted by the National Institute of Dental and Craniofacial Research in the United States between 1986 and 1987 and by the Centers for Disease Control between 1999 and 2004 was the only national data source on dental fluorosis prevalence. Prior to the 1999-2004 study published, the CDC published a provisional report covering data from 1999 to 2002.
The US Centers for Disease Control found a 9 percentage point increase in the prevalence of dental fluorosis confirmed in the 1999-2002 study in American children and adolescents than was found in similar surveys from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African-Americans suffer from higher levels of fluorosis than Caucasian Americans.
This condition is more common in rural areas where drinking water comes from shallow wells or hand pumps. It is also more likely to occur in areas where drinking water has a fluoride content of more than 1 ppm (parts per million).
If the water supply is fluoridated at 1 ppm, one should consume one liter of water to take 1 mg of fluoride. It is unlikely that a person will receive more than the tolerable upper limit of consuming optimal fluoride water alone.
Fluoride consumption may exceed the tolerable upper limit when a person drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoride toothpaste, consuming foods with high fluoride content, or taking fluoride supplements. The use of fluoride supplementation as a precaution for tooth decay was rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.
Tooth fluorosis can be prevented by lowering the amount of fluoride intake into the upper limits that can be tolerated.
In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone but a dental health care professional to see, can result from ingesting more optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix formula; and that the chances of the infant having fluorosis can be reduced by using a ready-to-eat infant formula or using fluoride-free or fluoride-free water to prepare a powder or liquid concentrate formula. They went on to say that how to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family doctor can help you determine how to optimize your child's fluoride intake."
History
In ancient times, Galen explained what perceived dental fluorosis. However, it was only in the early twentieth century that dental fluorosis was increasingly recognized and studied scientifically.
In 1901 Eager published the first description of "dozens" of elliptical immigrants from a small village near Naples, Italy. He writes that this condition is called "Denti di Chiaie" (Chiaie tooth), named after Stefano Chiaie, an Italian professor. In the United States, a dentist, Frederick McKay, began training in Colorado Springs in 1901 and found most of the population had stained teeth, locally called "Colorado brown stains". He brought this information to Greene Vardiman Black, a prominent American dentist at the time. After examining the affected email specimen, in 1916 Black described the condition as "[a] endemic endemic n of dental enamel, hitherto unknown in dentistry literature." They made an interesting observation that although freckled emails were hypomineralized, and therefore should be more susceptible to decay, this did not happen. Gradually, they become aware of existing reports and more about similar conditions around the world.
In 1931, 3 different groups of scientists around the world published their findings that this condition was caused by fluoride in drinking water during childhood. This condition then began to be called "dental fluorosis". Through epidemiological studies in the United States, Henry Trendley Dean helps identify the causal link between high fluoride concentrations in drinking water and freckles. He also produced a classification system for dental fluorosis still used in modern times, Dean's Index. As a follow-up study, the effect of fluoride protection against tooth decay is indicated.
References
Source of the article : Wikipedia
0 Comments