Ajay Kumar at 17:46, 29 August 2023

2023-08-29T17:46:23Z

New page

{{Infobox medical condition (new)
| name = Dental fluorosis
| synonyms = Mottled enamel<ref name="Dean2015">{{cite book | vauthors = Dean JA |title=McDonald and Avery's Dentistry for the Child and Adolescent|url=https://books.google.com/books?id=HqtcCgAAQBAJ&pg=PT132|edition=10th|date=10 August 2015|publisher=Elsevier Health Sciences|isbn=978-0-323-28746-3|page=132}}</ref>
| image = Dental fluorosis (mild).png
| caption = Mild fluorosis: in its usual mildest form, fluorosis appears as opaque white patches on the enamel
| pronounce =
| field = [[Dentistry]]
| symptoms =
| complications =
| onset =
| duration =
| types =
| causes =
| risks =
| diagnosis =
| differential =
| prevention =
| treatment =
| medication =
| prognosis =
| frequency =
| deaths =
}}

'''Dental fluorosis''' is a common<ref name="Neville2015">{{cite book | vauthors = Neville BW, Chi AC, Damm DD, Allen CM |title=Oral and Maxillofacial Pathology|url=https://books.google.com/books?id=Qs-JCgAAQBAJ&pg=PA52|edition=4th|date=13 May 2015|publisher=Elsevier Health Sciences|isbn=978-1-4557-7052-6|pages=52–54}}</ref> disorder, characterized by [[Enamel hypocalcification|hypomineralization]] of [[tooth enamel]] caused by ingestion of excessive [[fluoride]] during enamel formation.<ref name=Wong2010>{{cite journal | vauthors = Wong MC, Glenny AM, Tsang BW, Lo EC, Worthington HV, Marinho VC | title = Topical fluoride as a cause of dental fluorosis in children | journal = The Cochrane Database of Systematic Reviews | issue = 1 | pages = CD007693 | date = January 2010 | volume = 2010 | pmid = 20091645 | doi = 10.1002/14651858.CD007693.pub2 | pmc = 8078481 }}</ref>

It appears as a range of visual changes in enamel<ref name="Berg2015">{{cite book | vauthors = Bergc JH, Slayton RL |title=Early Childhood Oral Health|url=https://books.google.com/books?id=OBcFCAAAQBAJ&pg=PA113|date=26 October 2015|publisher=John Wiley & Sons|isbn=978-1-118-79210-0|page=113}}</ref> causing degrees of [[Tooth discoloration#Intrinsic discoloration|intrinsic tooth discoloration]], and, in some cases, physical damage to the teeth. The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure.<ref name="Dean2015" /> The "very mild" (and most common) form of fluorosis, is characterized by small, opaque, "paper white" areas scattered irregularly over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently "disfigure" the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.<ref name="Dean2015" />

People with fluorosis are relatively resistant to [[dental caries]] (tooth decay caused by bacteria),<ref name="Neville2015" /> although there may be cosmetic concern.<ref name="Neville2015" /> In moderate to severe fluorosis, teeth are weakened and suffer permanent physical damage.<ref name=Meiers2014>{{cite web|author1=Meiers P|title=HT Dean´s epidemiology of Mottled Teeth|url=http://www.fluoride-history.de/classification.htm|website=The History of Fluorine, Fluoride and Fluoridation|access-date=12 November 2015}}</ref>

==Diagnosis==
[[File:G amelogenesis imperfecta.jpg|thumbnail|Amelogenesis imperfecta: this condition can be mistaken for fluorosis]]The adequate diagnosis of fluorosis can be diagnosed by visual clinical examination. This requires inspection of dry and clean tooth surfaces under a good lighting.<ref name="fluorosisindex2015">{{cite web|url=http://fluorosisindex.com/about|title=E-training for Dean's Index Version 2|publisher=Oral Health Services Research Centre, University College Cork, Ireland.|access-date=12 November 2015|vauthors=Whelton H, Browne D, Felicia P, Whelton J|archive-url=https://web.archive.org/web/20160604074532/http://fluorosisindex.com/about|archive-date=4 June 2016|url-status=dead}}</ref> There are individual variations in clinical fluorosis manifestation which are highly dependent on the duration, timing, and dosage of fluoride exposure.There are different classifications to diagnose the severity based on the appearances. The clinical manifestation of mild dental fluorosis is mostly characterised a snow flaking appearance that lack a clear border, opaque, white spots, narrow white lines following the perikymata or patches as the opacities may coalesce with an intact, hard and smooth enamel surface on most of the teeth.<ref name="Abanto Alvarez">{{cite journal | vauthors = Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL | title = Dental fluorosis: exposure, prevention and management | journal = Medicina Oral, Patologia Oral y Cirugia Bucal | volume = 14 | issue = 2 | pages = E103–7 | date = February 2009 | pmid = 19179949 | url = http://medicinaoral.com/medoralfree01/v14i2/medoralv14i2p103.pdf }}</ref> With increasing severity, the subsurface enamel, all along the tooth becomes more porous. Enamel may appear yellow/ brown discolouration and/ or many and pitted white-brown lesions that look like cavities. They are often described as "mottled teeth".<ref>{{cite journal | vauthors = Ritter AV | title = Dental fluorosis | journal = Journal of Esthetic and Restorative Dentistry | volume = 17 | issue = 5 | pages = 326–7 | year = 2005 | pmid = 16225799 | doi = 10.1111/j.1708-8240.2005.tb00139.x }}</ref> Fluorosis does not cause discolouration to the enamel directly, as upon eruption into the mouth, affected permanent teeth are not discoloured yet. In dental enamel, fluorosis causes subsurface porosity or [[hypomineralization]]s, which extend toward the dentinal-enamel junction as the condition progresses and the affected teeth become more susceptible to staining. Due to diffusion of [[exogenous ion]]s (e.g., iron and copper), stains develop into the increasingly and abnormally porous enamel.<ref name="Abanto Alvarez" />

[[File:Enamel celiac.jpg|thumb|Enamel hypoplasia caused by untreated celiac disease: this condition is often confused with fluorosis<ref name="NIH">[http://celiac.nih.gov/PDF/Dental_Enamel_Defects_508.pdf Dental Enamel Defects and Celiac Disease] {{webarchive|url=https://web.archive.org/web/20160305124250/http://celiac.nih.gov/PDF/Dental_Enamel_Defects_508.pdf|date=March 5, 2016}} National Institute of Health (NIH)</ref>]]

The [[differential diagnosis]] for this condition includes:
* [[Turner's hypoplasia]] (although this is usually more localized)
* Enamel defects caused by an undiagnosed and untreated [[coeliac disease|celiac disease]].<ref name="NIH" />
* Some mild forms of [[amelogenesis imperfecta]] and [[enamel hypoplasia]]
* Enamel defects caused by infection of a primary tooth predecessor
* [[Tooth decay|Dental caries]]: Fluorosis-resembling enamel defects are often misdiagnosed as dental caries.<ref>{{cite journal | vauthors = Sabokseir A, Golkari A, Sheiham A | title = Distinguishing between enamel fluorosis and other enamel defects in permanent teeth of children | journal = PeerJ | volume = 4 | pages = e1745 | date = 2016-02-25 | pmid = 26966672 | pmc = 4782718 | doi = 10.7717/peerj.1745 }}</ref>
* [[Dental trauma]]: Mechanical trauma to the primary tooth may cause disturbance to the maturation phase of enamel formation, which may result in enamel opacities on the permanent successors.<ref>{{cite journal | vauthors = Skaare AB, Maseng Aas AL, Wang NJ | title = Enamel defects in permanent incisors after trauma to primary predecessors: inter-observer agreement based on photographs | journal = Dental Traumatology | volume = 29 | issue = 2 | pages = 79–83 | date = April 2013 | pmid = 22676308 | doi = 10.1111/j.1600-9657.2012.01153.x }}</ref>

==Classification==
[[File:4724507933 07ac954c27 bFluorose.jpg|thumbnail|Severe fluorosis: brown discolored and mottled enamel of an individual from a region with high levels of naturally occurring fluoride]]
[[File:FluorosisFromNIH.jpg|thumbnail|Severe fluorosis: the enamel is pitted and discolored]]
The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al. 1984), which combines Deans index and the TF index; and the fluorosis risk index (Pendrys 1990), which is intended to define the time at which fluoride exposure occurs, and relates fluorosis risk with tooth development stage.<ref name=Fejerskov2009 />

===Dean's index===
Dean's fluorosis index was first published in 1934 by [[H. Trendley Dean]]. The index underwent two changes, appearing in its final form in 1942.<ref name=Meiers2014/> An individual's fluorosis score is based on the most severe form of fluorosis found on two or more teeth.<ref name=fluorosisindex2015 />
{| class="wikitable"
|+
! Classification !! Code !! Criteria – description of enamel
|-
|Normal||0||The enamel represents the usual translucent semivitriform (glass-like) type of structure. The surface is smooth, glossy and usually of pale creamy white color
|-
|Questionable||1||The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to occasional white spots. This classification is utilised in those instances where a definite diagnosis is not warranted and a classification of 'normal' not justified
|-
|Very Mild||2||Small, opaque, paper white areas scattered irregularly over the tooth but not involving as much as approximately 25% of the tooth surface. Frequently included in this classification are teeth showing no more than about 1 – 2mm of white opacity at the tip of the summit of the cusps, of the bicuspids or second molars.
|-
|Mild||3||The white opaque areas in the enamel of the teeth are more extensive but do involve as much as 50% of the tooth.
|-
|Moderate||4||All enamel surfaces of the teeth are affected and surfaces subject to attrition show wear. Brown stain is frequently a disfiguring feature
|-
|Severe||5||All enamel surfaces are affected and hypoplasia is so marked that the general form of the tooth may be affected. The major diagnostic sign of this classification is discrete or confluent pitting. Brown stains are widespread and teeth often present a corroded-like appearance.
|-
|}

===TF index===
Proposed by Thylstrup and Fejerskov in 1978, the TF index represents a logical extension of Dean's index, incorporating modern understanding of the underlying pathology of fluorosis.<ref name="Fejerskov2009" /> It scores the spectrum of fluorotic changes in enamel from 0 to 9, allowing more precise definition of mild and severe cases.<ref>{{Cite book|title=Health effects of ingested fluoride|last=Wagner|first=Bernard Meyer | name-list-style = vanc |publisher=Washington, D.C. : National Academy Press|year=1993|isbn=9786610211333|page=171}}</ref>

==Causes==
Dental fluorosis is caused by a higher than normal amount of fluoride ingestion whilst teeth are forming. Primary dentine fluorosis and enamel fluorosis can only happen during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance which is due to the surface of the enamel being hypomineralised.<ref name=":1">{{cite book |vauthors=Denbesten P, Li W |chapter=Chronic fluoride toxicity: dental fluorosis |veditors=Buzalaf MA |title=Fluoride and the Oral Environment |pages=81–96 |date=2011 |pmid=21701193 |pmc=3433161 |doi=10.1159/000327028 |series=Monographs in Oral Science, Vol. 22 |volume=22 |isbn=978-3-8055-9659-6}}</ref>

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life.<ref>{{cite journal | vauthors = Hong L, Levy SM, Broffitt B, Warren JJ, Kanellis MJ, Wefel JS, Dawson CV | year = 2006 | title = Timing of fluoride intake in relation to development of fluorosis on maxillary central incisors | journal = Community Dentistry and Oral Epidemiology | volume = 34 | issue = 4| pages = 299–309 | doi=10.1111/j.1600-0528.2006.00281.x| pmid = 16856950 }}</ref><ref>Buzalaf MAR, Levy SM (2011): Fluoride intake of children: considerations for dental caries and dental fluorosis in Fluoride and the Environment. Editor: MAR Buzalaf, Karger, Basel. Pages 1-19</ref> From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride.<ref>{{Cite web|url = http://www.bfsweb.org/onemillion/05%20One%20in%20a%20Million%20-%20Dental%20Fluorosis.pdf|title = Dental Fluorosis}}</ref> The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth.<ref name="Alvarez">{{cite journal | vauthors = Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL | title = Dental fluorosis: exposure, prevention and management | journal = Medicina Oral, Patologia Oral y Cirugia Bucal | volume = 14 | issue = 2 | pages = E103–7 | date = February 2009 | pmid = 19179949 | url = http://medicinaoral.com/medoralfree01/v14i2/medoralv14i2p103.pdf }}</ref> Individual susceptibility to fluorosis is also influenced by genetic factors.<ref name="Clark2014">{{cite journal | vauthors = Clark MB, Slayton RL | title = Fluoride use in caries prevention in the primary care setting | journal = Pediatrics | volume = 134 | issue = 3 | pages = 626–33 | date = September 2014 | pmid = 25157014 | doi = 10.1542/peds.2014-1699 | doi-access = free }}</ref>

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public [[water fluoridation]].<ref name=EPA>{{cite web |title= Comment-Response Summary Report for the Peer Review of the Fluoride: Dose-Response Analysis for Non-Cancer Effects Document |year=2010 |url=http://water.epa.gov/action/advisories/drinking/upload/EPA_comments11-5-2010.pdf |website=Environmental Protection Agency |id=820-R-10-016}}</ref> The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic.<ref name=EPA/><ref name=Yeung>{{cite journal | vauthors = Yeung CA | title = A systematic review of the efficacy and safety of fluoridation | journal = Evidence-Based Dentistry | volume = 9 | issue = 2 | pages = 39–43 | year = 2008 | pmid = 18584000 | doi = 10.1038/sj.ebd.6400578 |doi-access=free}}
*{{cite web |date=2007 |title=NHMRC Public Statement: The Efficacy and Safety of Fluoridation 2007 |website=National Health and Medial Research Council |url=http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/eh41_statement_efficacy_safety_fluoride.pdf |archive-url=https://web.archive.org/web/20140213000930/http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/eh41_statement_efficacy_safety_fluoride.pdf |archive-date=2014-02-13}}</ref> Severe cases can be caused by exposure to water that is naturally fluoridated to levels above the recommended levels, or by exposure to other fluoride sources such as [[Tea brick|brick tea]] or pollution from high fluoride coal.<ref>{{cite book |chapter= Environmental occurrence, geochemistry and exposure |title= Fluoride in Drinking-water |vauthors=Fawell J, Bailey K, Chilton J, Dahi E, Fewtrell L, Magara Y |publisher= World Health Organization |isbn=92-4-156319-2 |year=2006 |chapter-url=https://www.who.int/water_sanitation_health/publications/fluoride_drinking_water_full.pdf |access-date=2009-01-24 |pages=5–27}}</ref>

Dental fluorosis has been growing in the United States concurrent with fluoridation of municipal water supplies, although disproportionately by race.<ref>{{cite journal|vauthors=Beltrán-Aguilar ED |display-authors=etal |title=Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis — United States, 1988–1994 and 1999–2002|journal=Morbidity and Mortality Weekly Report. Surveillance Summaries|date=August 26, 2005|volume=54 | issue=3 |pages=1–44 | url=https://www.cdc.gov/mmwr/preview/mmwrhtml/ss5403a1.htm |pmid=16121123}}</ref> A 2010 CDC report acknowledges an overall incidence of dental fluorosis of 22% from 1986-87 increased to 41% in the early 21st century, with an increase in moderate to severe dental fluorosis from 1% to 4%.<ref>{{cite journal |pmid=21211168 |url=https://www.cdc.gov/nchs/data/databriefs/db53.pdf |year=2010 |last1=Beltrán-Aguilar |first1=E. D |title=Prevalence and severity of dental fluorosis in the United States, 1999-2004 |journal=NCHS Data Brief |issue=53 |pages=1–8 |last2=Barker |first2=L |last3=Dye |first3=B. A }}</ref> The 2011-12 [[National Health and Nutrition Examination Survey|NHANES]] figures documented another 31% overall increase among American teens since the previous decade, with a total adolescent population impact of 61% afflicted. More than one in five American teens (23%) have moderate to severe dental fluorosis on at least two teeth.<ref>{{cite journal |pmid=29500282 |pmc=5929463 |year=2018 |last1=Wiener |first1=R. C |title=Dental Fluorosis over Time: A comparison of National Health and Nutrition Examination Survey data from 2001-2002 and 2011-2012 |journal=Journal of Dental Hygiene |volume=92 |issue=1 |pages=23–29 |last2=Shen |first2=C |last3=Findley |first3=P |last4=Tan |first4=X |last5=Sambamoorthi |first5=U }}</ref>

==Mechanism==
Teeth are the most studied body tissues to examine the impact of fluoride to human health. There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiate the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluoride interacts with mineralising tissues<ref>{{Cite journal |last=Kidd |first=E.A.M. |date=2004 |title=How ‘Clean’ Must a Cavity Be before Restoration? |url=https://www.karger.com/Article/FullText/77770 |journal=Caries Research |language=en |volume=38 |issue=3 |pages=305–313 |doi=10.1159/000077770 |issn=0008-6568|doi-access=free }}</ref>.<ref>{{cite journal |doi=10.1177/154411130201300206 |pmid=12097358 |title=Dental Fluorosis: Chemistry and Biology |journal=Critical Reviews in Oral Biology & Medicine |volume=13 |issue=2 |pages=155–70 |year=2016 |last1=Aoba |first1=T |last2=Fejerskov |first2=O }}</ref>

In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins ([[amelogenin]]) are enzymatically broken down and the rate at which the subsequent breakdown products are removed.<ref name="Neville2015" /><ref name="Fejerskov2009" /> Fluoride may also indirectly alter the action of [[protease]] via a decrease in the availability of free calcium ions in the mineralization environment.<ref name="Fejerskov2009" /> This results in the formation of enamel with less mineralization. This hypomineralized enamel has altered optical properties and appears opaque and lusterless relative to normal enamel.<ref name="Neville2015" />

Traditionally severe fluorosis has been described as [[enamel hypoplasia]], however, hypoplasia does not occur as a result of fluorosis.<ref name=Fejerskov2009 /> The pits, bands, and loss of areas of enamel seen in severe fluorosis are the result of damage to the severely hypomineralized, brittle and fragile enamel which occurs after they erupt into the mouth.<ref name=Fejerskov2009 />

[[Hydroxyapatite]] is converted to fluoroapatite in a [[fluorapatite|three step process]]. Dental fluorosis can be prevented at a population level through [[defluoridation]]. It is the downward adjustment of the level of [[fluoride]] in drinking water.

==Management==
Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:
* Mild cases: [[Tooth bleaching]]<ref name=":1" />
* Moderate cases: [[Enamel microabrasion]] (outer affected layer of enamel is abraded in an acidic environment)<ref name=":1" />
* Severe cases: [[Composite filling]]s, Micro-abrasion, [[Veneer (dentistry)|Veneer]]s, [[Crown (dentistry)|Crown]]s<ref name=":1" />

== Epidemiology==
Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control.<ref name="cdc.gov">{{cite journal|url=https://www.cdc.gov/nchs/data/databriefs/db53.pdf |title=Prevalence and Severity of Dental Fluorosis in the United States, 1999–2004 |first1=Eugenio D.|last1=Beltrán-Aguilar |first2=Laurie|last2=Barker |first3=Bruce A.|last3=Dye |journal=NCHS Data Brief |id=NCHS data brief, no 53 |publisher=[[National Center for Health Statistics]] |date=2010 |issue=53 |pages=1–8 |pmid=21211168 |access-date=2011-04-26 |url-status=live |archive-url=https://web.archive.org/web/20160616154209/http://www.cdc.gov/nchs/data/databriefs/db53.pdf |archive-date=2016-06-16 }}</ref>
{{As of|2005}} surveys conducted by the [[National Institute of Dental and Craniofacial Research]] in the USA between 1986 and 1987<ref name="ADA2">{{cite book|title=Fluoridation Facts| url=http://www.ada.org/~/media/ADA/Member%20Center/FIles/fluoridation_facts.ashx| year=2005| publisher=American Dental Association|format=PDF| page=29}}{{cbignore|bot=medic}}</ref> and by the [[Center of Disease Control]] between 1999 and 2004<ref name="cdc.gov"/> are the only national sources of data concerning the prevalence of dental fluorosis. Before the 1999-2004 study was published, CDC published an interim report covering data from 1999 to 2002.<ref name="CDC2002">{{Cite web|url=https://www.cdc.gov/mmwr/preview/mmwrhtml/ss5403a1.htm#tab23|title=Table 23, Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999--2002|access-date = 2006-10-29|publisher=Centers for Disease Control and Prevention|year=2005}}</ref>

{| class="wikitable"
|+ CDC findings on children and adolescents
|-
!bgcolor="#aaaaaa"|Deans Index
!bgcolor="#aaaaaa"|2002
|-
|Questionable fluorosis||11.5%
|-
|Very mild fluorosis||21.68%
|-
|Mild fluorosis||6.59%
|-
|Moderate to severe fluorosis||3.26%
|-
|Total confirmed fluorosis prevalence||31.65%
|-
|Total confirmed and questionable fluorosis prevalence||43.15%
|}

The U.S. Centers for Disease Control found a [https://www.cdc.gov/mmwr/preview/mmwrhtml/ss5403a1.htm 9 percentage point increase in the prevalence of confirmed dental fluorosis] in a 1999-2002 study of American children and adolescents than was found in a similar survey 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 rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps. {{Citation needed|date=April 2013}} It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

{| class="wikitable"
|+ Dietary reference intakes for fluoride<ref name="ADA2"/>{{rp|25}}
|-
! Age group
! Reference weight kg (lb)
! Adequate intake (mg/day)
! Tolerable upper intake (mg/day)
|-
| Infants 0–6 months
| 7 (16)
| 0.01
| 0.7
|-
| Infants 7–12 months
| 9 (20)
| 0.5
| 0.9
|-
| Children 1–3 years
| 13 (29)
| 0.7
| 1.3
|-
| Children 4–8 years
| 22 (48)
| 1.0
| 2.2
|-
| Children 9–13 years
| 40 (88)
| 2.0
| 10
|-
| Boys 14–18 years
| 64
(142)
| 3.0
| 10
|-
| Girls 14–18 years
| 57 (125)
| 3.0
| 10
|-
| Males 19 years and over
| 76 (166)
| 4.0
| 10
|-
| Females 19 years and over
| 61 (133)
| 3.0
| 10
|}

If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s. 

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 except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed [[infant formula]] or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way 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 physician can help you determine how to optimize your child's fluoride intake."<ref>[http://www.ada.org/4052.aspx Frequently Asked Questions (FAQ), American Dental Association Website accessed February 4, 2012] {{webarchive |url=https://web.archive.org/web/20160112124533/http://www.ada.org/4052.aspx |date=January 12, 2016 }}</ref>

==Prevention==
Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit. This can be achieved by consuming de-fluorinated water and improving the general nutritional status of the people.<ref>{{cite web|url=https://www.aimu.us/2017/08/15/fluorosis-causes-diagnosis-management-and-prevention/|title=Fluorosis: Causes, Diagnosis, Management and Prevention|date=August 15, 2017|website=AIMU.us}}</ref>{{bsn|date=July 2021}}

==History==

In ancient times, [[Galen]] describes what is thought to be dental fluorosis.<ref name="Fejerskov2009">{{cite book | vauthors = Fejerskov O, Kidd E | title=Dental Caries: The Disease and Its Clinical Management|url=https://books.google.com/books?id=fZfXWhSmG1UC&pg=PA299|date=16 March 2009|publisher=John Wiley & Sons|isbn=978-1-4443-0928-7|pages=299–327}}</ref> However, it was not until the early 20th century that dental fluorosis became increasingly recognized and scientifically studied.

In 1901 Eager published the first description of the "mottled enamel" of immigrants from a small village near Naples, Italy.<ref name=Eager1901>{{cite journal|author1=Eager JM|title=Denti di Chiaie (Chiaie teeth)|journal=Public Health Reports|date=November 1, 1901|volume=16|issue=44|pages=2576–2577}} Reprinted in {{cite journal | title = Public Health Reports, November 1, 1901: Denti di Chiaie (Chiaie teeth), by J.M. Eager | journal = Public Health Reports | volume = 91 | issue = 3 | pages = 284–5 | year = 1976 | pmid = 818673 | pmc = 1438998 }}</ref> He writes that the condition is called "Denti di Chiaie" (Chiaie teeth), named after Stefano Chiaie, an Italian professor.<ref name=Eager1901 /> In the United States of America, a dentist, [[Frederick McKay]], set up practice in Colorado Springs in 1901 and discovered a high proportion of the residents had stained teeth, locally termed the "Colorado brown stain".<ref name=Fejerskov2009 /> He took this information to [[Greene Vardiman Black]], a prominent American dentist of the time. After examining specimens of affected enamel, in 1916 Black described the condition as "[a]n endemic imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry."<ref name=Fejerskov2009 /> They made the interesting observation that although the mottled enamel was hypomineralized, and therefore should be more susceptible to decay, this was not the case.<ref name=Fejerskov2009 /> Gradually, they became aware of existing and further reports of a similar condition worldwide.<ref name=Fejerskov2009 />

In 1931, 3 different groups of scientists around the world published their discoveries that this condition was caused by fluoride in drinking water during childhood.<ref>{{cite journal| vauthors = Velu H, Balozet L|title=Reproduction experimentale chez Ie mouton de la dystrophie dentaire des animaux des zones phosphates|journal=Bull Acad Vet France|date=1931|volume=4|pages=373}}</ref><ref>{{cite journal|last1=Churchill HV|title=Occurrence of fluorides in some water of the United States|journal=Ind Eng Chem|date=1931|volume=23|issue=9|pages=996–998|doi=10.1021/ie50261a007}}</ref><ref>{{cite journal | vauthors = Smith MC, Lantz EM, Smith HV | journal = Science | volume = 74 | issue = 1914 | pages = 244 | date = September 1931 | pmid = 17755565 | doi = 10.1126/science.74.1914.244 | bibcode = 1931Sci....74..244C | title = The Cause of Mottled Enamel }}</ref><ref name=Teotia1999>{{cite journal | vauthors = Teotia SP | title = Dental fluorosis | journal = The National Medical Journal of India | volume = 12 | issue = 3 | pages = 96–8 | date = 1999 | pmid = 10492579 | url = http://www.nmji.in/archives/Volume-12/issue-3/editorials-2.pdf | archive-url = https://web.archive.org/web/20160304123429/http://www.nmji.in/archives/Volume-12/issue-3/editorials-2.pdf | url-status = dead | archive-date = 2016-03-04 }}</ref> The condition then started to become termed "dental fluorosis".<ref name=Teotia1999 /> Through epidemiological studies in the US, [[Henry Trendley Dean]] helped to identify a causal link between high concentrations of fluoride in the drinking water and mottled enamel.<ref name=Fejerskov2009 /> He also produced a classification system for dental fluorosis that is still used in modern times, Dean's Index.<ref name=Fejerskov2009 /> As research continued, the protective effect of fluoride against dental decay was demonstrated.<ref name=Fejerskov2009 />

==See also==
* [[Skeletal fluorosis]]
* [[Fluoride toxicity]]

== References ==
{{Reflist}}

== External links ==
{{Medical resources
| DiseasesDB =
| ICD10 = {{ICD10|K|00|3|k|00}}
| ICD9 = {{ICD9|520.3}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj =
| eMedicineTopic =
| MeshID =
}}
{{Oral pathology}}
{{Authority control}}

[[Category:Developmental tooth disorders]]
[[Category:Toxic effects of dietary elements]]
[[Category:Fluorine]]

Dental fluorosis - Revision history

Ajay Kumar at 17:46, 29 August 2023