Dental fluorosis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
K00.3 Mottled teeth;
Dental fluorosis;
Spotted enamel
ICD-10 online (WHO version 2019)
Mild form of dental fluorosis

Dental fluorosis , (also: Dentalfluorose , Colorado Brown Stain or Texas Teeth ; from fluorine and -ose, ancient Greek -ωσις , medicine: mostly a non-inflammatory disease; English : Mottled teeth or mottling , speckled teeth), is caused by excessive fluoride intake during the ontogenetic development of teeth .

While fluoride mg in a dosage of about 1 / day as an effective means for prevention of caries ( fluoridation is considered), it generates the dental fluorosis in higher doses, in which white to brown discolorations in the form of spots or stripes on the enamel surface form. Occasionally the entire tooth surface is discolored chalk white (matt) and interspersed with brown discoloration. To a greater extent, this is not only cosmetically disruptive, but also harmful to the teeth, since the enamel surface becomes less resistant as a result.

Basics

Hydroxyapatite forms the basis of the hard substance of all vertebrates . It is contained in bones to a proportion of about 40%, in the dentine to 70% and in the enamel (enamelum) to 97%. Tooth enamel is made up of adamantoblasts (ameloblasts, enamel- forming cells). These cells first secrete a connective tissue substance (prenamelum). After the tooth eruption, the main part of the mineralization takes place: the tooth enamel attains its final hardness through the storage of Ca 2+ ions and phosphates in the form of apatite .

If tooth enamel is brought into solution at a pH <5.5, it demineralizes. This happens in the mouth through bacterial acids and fruit acids , whereby ionic calcium, phosphate and water are formed from hydroxyapatite under the influence of acids:

Ca 5 (PO 4 ) 3 (OH) + H 3 O + → 5 Ca 2+ + 3 (PO 4 ) 3- + 2H 2 O

Intoxication with trace elements

Unit cell of fluorapatite

Professional exposure to phosphorus , lead , bismuth , strontium and fluorine can trigger toxic osteopathies with hyperostosis and cancellous sclerosis. In animal experiments, changes to the teeth have been found with the administration of cadmium salts, as in fluorosis, as well as influences on the iron metabolism (as well as after fluoride feeding). In humans, permanent tooth damage caused by these substances can only come into question if they are exposed to them during the development of the teeth. This means that intoxications are limited to strontium and fluorine in drinking water as well as to overdosing fluoride preparations. The dose-dependent influence of the strontium content in drinking water has so far been little studied. With an increasing level of 0.2–34.0 mg / l strontium, there is a correlation to the increase in line-shaped hypoplasia (horizontal enamel streaking) even if fluorosis can be excluded.

Fluoridation

During fluoridation , hydroxyapatite is converted to fluorapatite :

Ca 5 (PO 4 ) 3 (OH) + F - → Ca 5 (PO 4 ) 3 F + OH -

Fluorapatite has a much lower solubility product at the same pH value , i.e. H. it dissociate far less fluorapatite molecules in a solution as Hydroxylapatitmoleküle. This is the reason why fluoroapatite is more stable than the body's own hydroxyapatite.

root cause

Fluoride is an enzyme inhibitor . The ameloblasts, which are only active during tooth development, are particularly sensitive. This is completed by the age of eight. Therefore, a cell-damaging effect of fluorides in humans in the form of typical tooth changes is only visible if they act during the growth phase. If the supply of fluoride is increased, the ameloblasts will not perform well in their synthesis and this will lead to a patchy underdevelopment of the tooth enamel. Too high fluoride concentrations disrupt matrix secretion, matrix breakdown, enamel maturation and enamel mineralization. The result is hypo- and hypermineralized areas in the enamel and dentine . The longer and more concentrated the fluoride, the larger the hypomineralized zones. Clinically, this disruption of enamel formation manifests itself through increased porosity and color changes. The exact mechanisms are the subject of current research.

diagnosis

The diagnosis of dental fluorosis is mainly based on the clinical picture, i.e. the visible changes in the enamel. In a standard work for dental training from 2001 it is suggested: "The clinical diagnosis of fluorosis must be pronounced cautiously in order not to discredit the demonstrably successful caries prophylaxis with fluorides."

Differential diagnosis

Amelogenesis imperfecta can be confused with dental fluorosis
Enamel defects in celiac disease (gluten intolerance), no dental fluorosis.

Dental fluorosis must be differentiated from the following dental diseases:

Various theories, such as bisphenol A exposure, dioxins and furans from the environment, an existing vitamin D deficiency and infections with chickenpox are discussed as further causes of changes in the enamel.

therapy

Depending on the severity and the aesthetic impairment, the following therapies can be considered:

history

Soon after Jakob Berzelius, as a spa guest in Carlsbad, had detected bound hydrofluoric acid in the sparkling water there for the first time in 1822, spa guests were concerned that this acid, which also seemed to corrode the drinking glass used, could damage their teeth. They were appeased by saying that tooth enamel did not contain any silicate that could be dissolved by the hydrofluoric acid. Approx. 110 years later, fluoride in drinking water was recognized as the cause of endemic dental fluorosis and the effect of fluoride was initially erroneously attributed to an etching effect that made the affected tooth surfaces look like corroded.

The first person to describe dental fluorosis was most likely the dentist C. Kühns, who in 1888 gave a lecture on black spotted teeth in a family who had come over from Durango (Mexico) and who then belonged to his circle of patients. From this family he learned that such discoloration was very common in Durango. He made iron or manganese deposits responsible for the discoloration, which resembled the "caries nigra". This early report is unusual, because since Carl Wedl in 1870 in his book Pathology of Teeth saw brown enamel discoloration of unknown origin as a sign of dental caries, the occurrence of dental fluorosis is likely to have often been misinterpreted. Otherwise, attempts by the Munich surgeon Ludwig von Stubenrauch could have provided important clues as to the cause as early as 1904. The surgeon had fed dogs with sodium fluoride during tooth development and found, in addition to the skeletal changes typical of fluorosis, that they "without exception developed typical caries of the teeth with incorrect teeth positions". In the area around Naples (Italy) the inhabitants had "denti neri" (black teeth) or "denti scritti" (which looked as if they were labeled), which the locals attributed to the gas emissions of Vesuvius . John Eager, a doctor of the United States Public Health Service (USPHS) stationed in Naples, reported about it in 1901, where the tooth damage was called "Denti di Chiaie" (after a district of Naples, Chiaia). Eleven years earlier, the Italian doctor and mineralogist Arcangelo Scacchi had written about the fluoride content of the volcanic exhalations and the soils in the area - but no one thought of a connection with the tooth damage reported there later.

Fluorosis in a cow

The discoloration has also been described in the dry coastal regions of North Africa since 1923, where both locals, but especially herbivores , were affected. There the phenomenon was called "Le darmous" by the Moroccan veterinarian Henri Velu (1887–1973), who described it for the first time in 1922 and was able to prove experimentally that the cause was a very high fluoride content in drinking water after it had passed through phosphorite containing fluorine . The disease is also called Velu-Charnot-Spéder syndrome . Velu found that unwashed samples of straw and barley had a higher fluoride content than washed samples. The pronounced fluorosis in herbivores was more the result of the dust-contaminated feed with a high fluoride content than the inhalation of fluoride-containing dust. In contrast, endemic human fluorosis in the region resulted mostly from inhalation of fluoride-containing phosphate dust. Similar symptoms of fluorosis were found in Holland , Mexico, and many cities in the United States.

Fluorosis Research by Frederick Sumner McKay

In the health resort and gold prospector paradise of Colorado Springs , Frederick Sumner McKay made a surprising observation. The teeth of many residents had unsightly brown spots ( English : "mottled teeth" - speckled teeth). For an “Eastern national” this was strange, but the local dentists and doctors did not attach great importance to it, especially since the discoloration had no obvious effects on health. However, McKay wanted to find out the cause and devoted 30 years of his life to this arduous search. He suspected that there must be a connection with the drinking water , although it was initially unclear whether this water was missing something in particular or whether an undesirable component was to be blamed. The first thing he did was test the Colorado Springs water source, including arsenic , but didn't find anything unusual. He had tested other waters too; they showed some similarities and some differences, but nothing in particular. A decisive experience for Mckay was when he visited some Portuguese families who had immigrated from the islands of Brava and Fogo on the Cape Verde Islands to Nantucket , Massachusetts. McKay visited these people and found that the Brava natives had teeth with the ominous brown spots, but the Fogo natives did not. With the same environment and diet on the Cape Verde Islands, the only difference might just be their drinking water. He had similar experiences with other population groups, but he still had no explanation for it.

As early as 1925, McKay was so convinced of the idea that there must be some connection with the composition of the regional drinking water that he could in good conscience advise the Oakley , Idaho community to invest $ 35,000 in a change of water source for those found there To stop tooth damage for future generations. However, he was only able to achieve actual success eight years later. On the other hand, his experiences from 1927 with the city of Lake Elsinore ( California ), about 100 miles southeast of Los Angeles, were frustrating . All of the native residents there had dental fluorosis. The city lived from tourism, however, the hot springs, which also supplied the city with drinking water, were used by spa guests for drinking and bathing cures. The owners of the spa buildings opposed a change of water sources, although McKay believed that there were a greater number of them to choose from. The problem was only resolved decades later after violent (also political) disputes and great pressure.

A similar heated debate about the drinking water supply as in Elsinore developed during the 1930s in Chetopa , Kansas , where a local dentist, James Scott Walker, played a pivotal role as the leader in advocates for a switch to a lower-fluoride water supply. The change of source, for which Walker had to fight until 1939, came about here only after security problems had been raised. When, after this success, dentists in Kansas recognized other sources as problematic, the head of the dental department of the Kansas State Board of Health, Leon Kramer, demanded that the limit value for fluoride be set as high as possible in order to ensure the water supply of the cities also under economic aspects . He suggested 3 ppm as a limit value.

The breakthrough

The breakthrough for McKay's project came in 1931 with water tests carried out by Harry V. Churchill (1886–1967), chief chemist in the research laboratories of the Aluminum Company of America (ALCOA) in New Kensington . Churchill had come into contact with McKay in a roundabout way and had the drinking water of Bauxite ( Arkansas ) tested for trace elements . The reason was the suspicion that aluminum cookware made by this company could be responsible for the brown stains. This thesis was supported by the fact that in the affected areas in Colorado the water could absorb aluminum from the cryolite- containing soil, as well as from the bauxite ore that was mined in the city of bauxite. Churchill noted, to his relief, an increased fluoride content in the respective water. He then, under the seal of secrecy, had water samples sent to him from various areas via McKay, the fluoride content of which he examined. While the fluoride content of the water in some cities roughly correlated with the severity of the dental fluorosis found by McKay there, no endemic damage was observed with a fluoride content of less than 1 ppm . With the help of the chemist's results, McKay had finally found the long-sought differences in drinking water as the cause of dental fluorosis. This also resulted in the name Colorado brown stain for dental fluorosis.

It was up to the dentist Henry Trendley Dean , who dealt with the problem at the USPHS from the end of 1931, to quantitatively represent this connection . Dean had met with McKay before taking up his new job and obtained details from him.

The endemic occurrence of dental fluorosis was first reported in Germany in the 1950s. Walter Hoffmann-Axthelm , then senior physician at Wolfgang Rosenthal's institute at the Humboldt University in Berlin, examined affected children in the Kneipp spa town of Berggießhübel from 1951 onwards.

Epidemiological Studies

In epidemiological studies, fluoride excretion is becoming increasingly important. It is assumed that around 50% of the amount of fluoride absorbed is excreted in the urine . Infants have very low levels of fluoride excretion. Diet-related factors and dental care products were important factors influencing fluoride excretion for small children. In 3-year-old test persons, the dental care habits had an influence on the fluoride excretion. Frequent tooth brushing with toothpaste containing fluoride is a relevant source of fluoride. Systemic prophylaxis means play a subordinate role among those over 3 years of age. With systemic prophylaxis, the highest values ​​of the individual fluoride excretion were found in the subjects who received pure fluoride preparations. If the fluoride excretion was lowest with the combination preparation, this is probably explained by an above-average retention in the fast-growing infants who received this combination. Regular and long-term systemic prophylaxis also resulted in higher levels of fluoride excretion.

Fluorosis indices

Moderate dental fluorosis
Severe form of dental fluorosis

Fluorosis indices were developed, on the one hand, to record the severity of the fluorosis depending on its severity and, on the other hand, to determine threshold values ​​for fluoride intake for caries prevention by means of epidemiological studies, at which no or tolerable fluorosis tooth damage occurs. When determining the individual fluoride intake, the total amount that is consumed daily from fluoride tablets, food, drinking water, other beverages (green and black tea (including iced tea), some mineral water, fluoridated milk), fluoridated table salt and fluoride-containing toothpastes must be determined.

Dean fluorosis index

H. Trendley Dean first published a fluorosis index in 1934. The index underwent two changes and was published in its final form in 1942. The severity depends on the most serious findings on two or more teeth.

Dean fluorosis index
Severity classification Symptoms Weighting
0 normal No changes 0
1 Questionable The enamel shows slight deviations in translucency, with occasional white
spots.		 0.5
2 Very mild Small, opaque, whitish areas, scattered irregularly over the tooth. There are
no longer involved in over 25 percent of the tooth surface.
This also includes teeth that have no more than about 1–2 mm of white opacity at the
cusp tips of the first or second molars.		 1
3 Mild Small, opaque, whitish areas, scattered irregularly over the tooth. No
more than 50 percent of the tooth surface is involved		 2
4th Medium difficulty All enamel surfaces of the teeth are affected. They show signs of abrasion and are
unsightly in appearance due to brown spots.		 3
5 Heavy All enamel surfaces are affected. The enamel hypoplasia are pronounced and appear
holey. The teeth show large brown enamel spots.		 3

Community Index of Dental Fluorosis

The Community Index of Dental Fluorosis (FCI) is often given in epidemiological studies on the prevalence of fluorosis and is calculated using the following formula, using the weighting in the Dean index shown above:

n = people suffering from fluorosis. w = weighting factor (severity), N = total number of all examined

Fluorosis index according to Thylstrup and Fejerskov

Upper canine tooth (tooth 13), in which the perikymatia (Retzius stripes: thin, parallel transverse lines) can be seen in full image resolution

In 1978 Thylstrup and Fejerskov developed a fluorosis index based on Deals Index. They included the underlying pathology of fluorosis. The index records changes in enamel on a scale from 0 to 9, so that a more precise definition of mild and severe cases is possible.

Fluorosis index according to Thylstrub and Fejerskov (TFI)
Severity Symptoms
0 No changes
1 Narrow white lines that follow the perikymatia
2 Narrow white lines that follow the perikymatia. Conference in a few places (snowcapping)
3 Pronounced white lines, confluent in a few places.
4th Pronounced white lines, confluent in most places.
5 Strongly merging lines with irregular, cloudy-opaque areas on the entire tooth surface.
6th Whole area with clear opacities or a chalky-white appearance <2 mm.
7th Opaque white or brownish surface with individual local hypoplasias
8th Surface melt loss in larger areas. The rest of the enamel is opaque in color.
9 Surface melt loss in larger areas. The tooth shape has changed.

TSIF index

Horowitz developed on the two previous indices to TSIF index (Tooth Surface Index of Fluorosis, Engl. : Tooth surface index at fluorosis) of the seven levels of severity provides.

Tooth Surface Index of Fluorosis (TSIF)
Severity Symptoms
0 No changes
1 The enamel shows clear evidence of fluorosis with areas of parchment-white color that
comprise less than a third of the visible enamel surface.
This category also includes teeth whose incisal edges of the front teeth or cusp tips of the
posterior teeth are affected ("snowcapping").
2 Parchment-white fluorosis that covers at least one third but less than two thirds of the visible surface.
3 Parchment-white fluorosis covering more than two thirds.
4th In addition to the appearances of the previous degrees of severity, the teeth are discolored from light brown to dark brown
5 The teeth have small, holey, rough, discolored defects that are surrounded by healthy tooth enamel
6th The teeth show both the described defects and extensive discoloration.
7th The teeth show confluent pitting of the enamel surface and large tooth enamel defects.
Dark brown spots are usually present.

Fluorosis Risk Index

The Fluorosis Risk Index (FRI; Engl. : Fluorosis risk index) was proposed in 1990 by Pendrys to be used in analytical epidemiological studies. It is used to more precisely identify age-specific requirements for fluoride administration and the resulting development of dental fluorosis. This index divides the enamel surfaces of the teeth in the permanent dentition into 2 groups.

Fluorosis Risk Index
category Tooth enamel formation Affected teeth
1 during the first year of life Incisal edges or occlusal surfaces of teeth 16, 11, 21, 26, 36, 31, 41, 46
( six-year molars and central incisors )
2 between the ages of three and six Cervical third of incisors,
middle third of canines 13, 23, 33, 43 and the
incisal and middle third of premolars and molars .

The findings are recorded in the respective categories according to the TFI fluorosis index according to Thylstrub and Fejerskov.

Calcification

Stages of tooth development

The following graphic overview shows the times at which the permanent teeth are calcified. Up to the complete enamel formation of the respective tooth, the formation of tooth fluorosis can occur due to the storage of fluorides in the event of an overdose. The perikymata ( so are) over the entire melting mantle distributed growth lines of the enamel . The course of the fluoridation damage can be classified according to age. The graphic shows the teeth of the upper left quadrant of the dentition, starting on the left with the central incisor ( tooth 21 ) and ending on the right with the upper left wisdom tooth ( tooth 28 ). The six-year-old molar ( tooth 26 ) calcifies first .

Tooth development: tooth .......... 21 ....................... 22 ............ ........... 23 ......................... 24 ............ ........... 25 ........................... 26 .......... .................... 27 ............................. 28
Tooth development in a five-year-old girl in the X-ray

Modified DDE index

In 1982, the Commission on Oral Health, Research and Epidemiology suggested the use of a Developmental defects of enamel index (DDE) before ( Engl. : Index of enamel developmental disorders). Due to its complexity, it was modified in 1989 by J. Clarkson and D. O'Mullane and has been recognized by the Fédération Dentaire Internationale (FDI), the world association of dentists, since 1999 .

Modified developmental defects of enamel index (DDE)
Severity Symptoms
0 normal
1 Limited opacities
2 Diffuse opacities
3 Hypoplasia
4th Hypoplasia with other defects
5 At the same time limited and diffuse opacities
6th Limited opacities with hypoplasia
7th Diffuse opacities with hypoplasia
8th Simultaneously limited and diffuse opacities with hypoplasia

Newer investigation methods

The Visual Analogue Scale (VAS) was developed in 2005 by Antonio Carlos Pereira. The laboratory study showed a better correlation between fluoride concentration and the VAS for dental fluorosis than between fluoride concentration and the TFI. Pretty and McGrady have been experimenting with quantitative light fluorescence (QLF) and, since 2012, with polarized light using a digital imaging system to capture images. The method should enable automated software analysis and be suitable for epidemiological studies.

literature

See also

Commons : Dental fluorosis  - album with pictures, videos and audio files

Individual evidence

  1. ↑ dental fluorosis (English)
  2. ↑ Hendrik Meyer-Lückel, Kim Ekstrand, Sebastian Paris: Caries: Science and Clinical Practice . Georg Thieme Verlag, 2012, ISBN 978-3-13-169321-1 , p. 200– ( google.com ).
  3. ↑ Robert H. Wilson, Floyd DeEds: Experimental chronic cadmium poisoning. Science 90 (1939) 498
  4. ^ Robert H. Wilson, Floyd deEds, Alvin J. Cox: Effects of continued cadmium feeding. J. Pharmacol. Exp. Ther. 71 (1941) 222
  5. ↑ Peter Dale, James T. Ginn, Joseph F. Volker: Some observations on the effect of cadmium on the dentition of the rat. J. dent. Res. 21 (1942) 302
  6. ↑ JT Ginn, Joseph F. Volker: Effect of cadmium and fluorine on the rat dentition. Proc. Soc. Exp. Biol. Med. 57 (1944) 189
  7. ↑ EV Pindborg, JJ Pindborg, CM Plum: Studies on incisor pigmentation in relation to liver iron and blood picture in the white rat. II. The effect of fluorine on the iron metabolism. Acta pharmacol. 2 (1946) 294
  8. ↑ EV Pindborg, JJ Pindborg, CM Plum: Studies on incisor pigmentation in relation to liver iron and blood picture in the white rat. IV. The relation between cadmium poisoning and iron metabolism. Acta pharmacol. 2 (1946) 302
  9. ↑ Joel Wisotzky, John W. Hein: The effects of solutions of cadmium sulphate and lead acetate on the incisor pigmentation, fur color, and blood in male and female Syrian Hamsters. J. dent. Res. 34 (1955) 768
  10. ↑ Peter Gängler: Conservative Dentistry and Periodontology: 66 tables . Georg Thieme Verlag, 2005, ISBN 3-13-593702-X , p. 74 ( google.com ).
  11. ↑ Eckhart Buddecke: Biochemical basics of dentistry . Walter de Gruyter, 1981, ISBN 3-11-008738-3 , p. 53-54 ( google.com ).
  12. ↑ Eckhart Buddecke: Biochemical basics of dentistry . Walter de Gruyter, 1981, ISBN 3-11-085820-7 , p. 83-84 ( google.com ).
  13. ↑ Ole Fejerskov, Edwina Kidd: Dental Caries: The Disease and Its Clinical Management . John Wiley & Sons, 2009, ISBN 978-1-4443-0928-7 , pp. 299 ff . ( google.com ). Retrieved June 4, 2016.
  14. ↑ Van Waes H. et al: Color Atlases of Dentistry: Pediatric Dentistry. 83 , Thieme, Stuttgart, 2001
  15. ↑ Jakob Berzelius: Extrait d'une lettre de M. Berzelius à M. Berthollet. In: Ann. de Chimie. 21, 1822, p. 246.
  16. ^ Joseph Ernest Ryba: Karlsbad and its healing springs. A handbook for spa guests. Kronberger and Weber Verlag, Prague 1828, pp. 127–128.
  17. ↑ Book review: Ryba: Carlsbad and its healing springs. In: Medicinal yearbooks of the imperial-royal Austrian state. NF 1st volume, 1829, p. 271.
  18. ^ FS McKay: letter of January 29, 1931 to HV Churchill; ALCOA papers, Wisconsin State Historical Society, Madison, Wisconsin
  19. ↑ German Mschr. Dentistry. 6, 1888, p. 446, cit. in: FJ McClure: Water Fluoridation. The search and the victory. NIDR, Bethesda, MD, 1970, pp. 1-3. Retrieved June 4, 2016.
  20. ↑ Ludwig von Stubenrauch: Experimental studies on the effect of fluorosodium on the bones, especially the jawbone. In: negotiation Dtsch Ges for surgery. 33rd Congress, Berlin, April 6, 1904, p. 20.
  21. ^ JM Eager: Denti di Chiaie (Chiaie Teeth). In: Publ Health Rep. Volume 16, 44, November 1, 1901, pp. 2576-2577.
  22. ↑ JM Eager: Chiaie Teeth. In: Periscope, Dental Cosmos. Volume 44, March 1902, pp. 300-303.
  23. ^ FJ McClure: Water Fluoridation. The search and the victory. NIDR, Bethesda, MD, 1970, pp. 1-3. Retrieved June 4, 2016.
  24. ^ Arcangelo Scacchi: La regione vulcanica fluorifera della Campania. G. Barbera, Firenze 1890.
  25. ↑ Gaston Compain: El Darmous'- Lésions of dents et ostéite you déformante maxillaire inférieur chez les animaux domestiques de la région du Gantour (Maroc). Thèse, Lyon 1926.
  26. ↑ Albert Claudon: Le Darmous. Dystrophy dentaire des espèces domestiques de la Haute-Chaouia. Thèse, Lyon 1931.
  27. ↑ Henri Velu: Le Darmous (ou Dermes) - fluorosis spontanée the zones phosphatées. In: Archives de l'institut Pasteur d'Algérie. 10: 1, Mar 1932, pp. 41-118.
  28. ↑ André Chambionnat: La lutte contre le Darmous. The dosage du fluor in the eaux. Son élimination en vue de la potabilité des eaux à Darmous. undated (approx. 1938)
  29. ↑ Y. Haikel, JC Birds, RM Frank: fluoride content of water, dust, soils and cereals in the endemic dental fluorosis area of Khouribga (Morocco). In: Archives of Oral Biology. 31, 1986, p. 279, doi: 10.1016 / 0003-9969 (86) 90041-5 .
  30. ^ P. Meiers: A new water supply for Oakley, Idaho. accessed on June 3, 2016.
  31. ^ FS McKay: Letter to Grover Kempf, USPHS, March 29, 1927; Ruth Roy Harris papers
  32. ↑ a b Hans Ludigs: Fluoride and the history of US dentistry. approx. 1900-1950 ; Master thesis. University of Konstanz, 2013.
  33. ^ J. Scott Walker: One Man's Battle Against Mottled Enamel. In: Oral Hygiene. March 24, 1934, pp. 340-347 .; American Journal of Public Health. January 23, 1933, pp. 47-48.
  34. ^ P. Meiers: The Bauxite Story. A look at Alcoa. Retrieved June 1, 2016.
  35. ↑ W. Hoffmann-Axthelm, R. Wohinz: First observations on the occurrence of dental fluorosis in Germany. Deutsche Stomatologie 2 (1952) p. 59
  36. ↑ Natasha Diller: Fluoride exposure of 0-6 year old children in Germany. Analyzes of urine samples from participants in the child and adolescent health survey. (KiGGS) , dissertation. 2011. Retrieved June 14, 2016.
  37. ↑ Gisoo Khorrami: Comparison of the caries and fluorosis prevalence in two areas with different drinking water fluoride content in Iran. Dissertation. FU Berlin, 2009. Retrieved June 13, 2016.
  38. ↑ P. Meiers: HT Dean's epidemiology of Mottled Teeth. In: The History of Fluorine, Fluoride and Fluoridation. Retrieved June 2, 2016 .
  39. ↑ H. Shelton, D. Browne, P. Felicia, J. Shelton: E-training for Dean's Index Version 2. Oral Health Services Research Center, University College Cork, Ireland., Archived from the original on June 4, 2016 ; accessed on June 2, 2016 .
  40. ↑ Thomas Weber: Dental fluorosis. In: Memorix Dentistry. 3. Edition. Thieme Verlag, 2010. Accessed June 5, 2016.
  41. ↑ A. Thylstrup, O. Fejerskov: Clinical appearance of dental fluorosis in permanent teeth in relation to histologic changes. In: Community dentistry and oral epidemiology. Volume 6, Number 6, November 1978, pp. 315-328. PMID 282114 .
  42. ↑ Elmar Hellwig, Joachim Klimek, Thomas Altin: Introduction to tooth preservation . Deutscher Ärzteverlag, 2009, ISBN 978-3-7691-3371-4 , p. 70 ( google.com ).
  43. ↑ Michael Bonnet: Diagnostic criteria for fluorosis: The TSIF Tooth Surface Index of Fluorosis. Fluoride Action Network, July 2012. Retrieved June 4, 2016.
  44. ↑ HS Horowitz et al .: A new method for assessing the prevalence of dental fluorosis - the Tooth Surface Index of Fluorosis. In: Journal of the American Dental Association. 109 (1), 1984, pp. 37-41.
  45. ↑ DG Pendrys: The fluorosis risk index: a method for investigating risk factors. In: Journal of public health dentistry. Volume 50, Number 5, 1990, pp. 291-298. PMID 2231522 (Review).
  46. ^ J. Clarkson, D. O'Mullane: A modified DDE Index for use in epidemiological studies of enamel defects. In: Journal of dental research. Volume 68, Number 3, March 1989, pp. 445-450. PMID 2921385 .
  47. ^ A review of developmental defects of enamel index (DDE). Federation Dentaire Internationale, Commission on Oral Health Research and Epidemiology. In: International Dental Journal. 42, 1992, pp. 411-426.
  48. ^ AP Vieira, HP Lawrence et al.: A visual analog scale for measuring dental fluorosis severity. In: Journal of the American Dental Association (1939). Volume 136, Number 7, July 2005, pp. 895-901. PMID 16060470 .
  49. ^ Iain A Pretty, Michael McGrady et al .: Quantitative Light Fluorescence (QLF) and Polarized White Light (PWL) assessments of dental fluorosis in an epidemiological setting. In: BMC Public Health. 12, 2012, p. 366, doi: 10.1186 / 1471-2458-12-366 .