Introduction
Early accounts of a distinctive Colorado brown stain were paramount to discovering the link between excessive fluoride ingestion and developing a hypoplastic dentition that would later be termed dental fluorosis.[1] Dental fluorosis is a common condition affecting both primary and secondary dentitions; however, the effects on secondary dentition are arguably more profound due to its permanency.[2]
The element fluorine is found most abundantly in its fluoride form in nature.[3] Certain geographical locations have relatively high naturally occurring fluoride concentrations in the water, for example, Pakistan, China, and India.[4] Excessive fluoride intake is associated with the development of pathological conditions, the impact of which is contingent on when the exposure occurs, the length of exposure, and the concentration of fluoride involved. Several conditions may develop depending on the abovementioned factors, including dental fluorosis, skeletal fluorosis, and fluoride toxicity.
The most common route of fluoride ingestion is via drinking water.[3] Alternative sources include plants, which similarly obtain fluorides through water uptake. Fluorides can also be inhaled. This occupational hazard is associated with mining and smelting metals, including aluminum.[5] Equally, fluoride deficiency is associated with deleterious effects, most notably an increased vulnerability to dental caries.[3]
The provision of systemic fluoride supplements, artificial water fluoridation, and the direct topical application of fluoride-containing dentifrices are preventative measures employed to reduce the risk of caries development.[6] These measures can also inadvertently lead to excessive fluoride intake and potentially cause dental fluorosis. The prevalence of dental fluorosis has increased significantly in the US and is estimated to be 65% in those aged 12-15 years, with 30.4% of diagnoses being classed as moderate to severe.[7]
Etiology
Register For Free And Read The Full Article
- Search engine and full access to all medical articles
- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Etiology
Dental fluorosis is caused by the excessive ingestion of fluoride during tooth development. The severity of dental fluorosis is dose-dependent and influenced by the extent of time an individual is exposed to excessive fluoride within the critical window of development and genetic factors.[8] Excessive plasma fluoride is believed to interfere with the removal of amelogenins during enamel maturation leading to the formation of hypomineralized enamel.[9]
The critical window for dental fluorosis to develop in response to excessive fluoride intake ranges from birth to eight years of age.[6] Thus, excessive consumption of fluoride outside of amelogenesis will not result in dental fluorosis. The visually detectable enamel changes characteristic of dental fluorosis are associated with water fluoride levels in excess of 1.5 ppm.[10]
Artificially fluoridated water has a target fluoride concentration of 1 ppm, which is thought to optimize the anti-cariogenic properties of fluoride while minimizing the risk of adverse effects, including dental fluorosis.[11]
Epidemiology
The worldwide prevalence of dental fluorosis is increasing.[12] In the US, 23% of the total population is affected. In adolescents, this increases to 41%, a figure which has almost doubled since 1987.[13] As a result of the significant increase in the prevalence of mild to moderate cases of dental fluorosis, the US Department of Health has reduced the target concentration in fluoridated water from 1ppm to 0.7 ppm.
It is important to note that although mild-moderate dental fluorosis is relatively common, clinically severe forms are rare in the US and Europe.[13][14] Dental fluorosis occurs equally in both genders and can occur in both primary and permanent dentition.[15][16]
Pathophysiology
Ameloblasts are responsible for enamel synthesis during amelogenesis, a tightly regulated process involving multiple phases in which hydroxyapatite crystals are produced.[17] The definitive pathophysiology of dental fluorosis is not fully understood.[18]
Exposure to high plasma fluoride levels during amelogenesis results in the formation of porous hypomineralized enamel.[10] In severe cases, the porosity can extend toward the dentino-enamel junction. The early maturation phase is the most vulnerable stage of amelogenesis to chronically elevated plasma fluoride levels.[17]
During the maturation phase, enamel matrix proteins, including amelogenin, are hydrolyzed by proteinases. This process is delayed in fluorosed enamel. Fluoride has also been shown to induce apoptosis in ameloblasts during enamel maturation which is thought to contribute to the enamel pitting found in severe cases of dental fluorosis.
History and Physical
Patients with dental fluorosis will have a history of chronic excessive fluoride ingestion within the critical window of amelogenesis. This is between birth and eight years of age.[6] Clinically the severity of dental fluorosis ranges from virtually undetectable surface-level enamel changes comprising of minute white opaque flecks, which the patient may be unaware of, to pitted enamel which becomes stained dark yellow-brown. Most patients will have aesthetic concerns bringing attention to the discoloration of their teeth.[19]
In mild and moderate cases, this is in the form of light enamel opacities.[20] In severe cases of dental fluorosis, they may also be concerned about structurally compromised enamel which becomes hypoplastic, a yellow-brown discoloration of the teeth, and occasionally dentine hypersensitivity.[19] Dental fluorosis has a symmetrical distribution, and the severity to which individual teeth are affected within the dentition can vary.[6]
Evaluation
A diagnosis of dental fluorosis is contingent on a positive fluoride history within the critical window of tooth development and a visual intraoral examination.[21] The utilization of effective lighting and a dental mirror is essential. Magnification can be a useful adjunct, especially in subtle cases of dental fluorosis. In cases where the surface enamel is pitted, a dental probe can be used carefully so as not to damage the already compromised tooth structure further. Radiographs and other dental investigations, such as sensibility testing, are of limited use where dental fluorosis is concerned.[22]
There is active research into tools to supplement the diagnosis of fluorosis, such as the use of short-wavelength infrared light. Under this spectrum, dental fluorosis appears in high contrast, which can help identify more subtle cases of fluorosis.[23] This also enables dental professionals to stage the grade of fluorosis more accurately. However, the use of these tools is not yet commonplace in clinical practice.
Treatment / Management
Where mild cases of dental fluorosis are concerned, involving subtle enamel changes, patients may be unaware or unconcerned with the appearance of their teeth. As such, no treatment may be necessary. Thus, treatment is patient-led where dental fluorosis is concerned, and patient concerns are cosmetic in most cases.[24] (A1)
Vital dental bleaching can be a highly effective treatment modality in mild cases of dental fluorosis. The concentration of hydrogen peroxide utilized varies between countries depending on legislation pertaining to the maximum permitted concentrations of hydrogen peroxide permissible for dental whitening.[25]
Generally, dental bleaching completed in a dental clinic will use a higher concentration than that provided to patients for at-home bleaching using bleaching trays. Lightening the healthy, unaffected tooth structure allows it to camouflage with lighter fluorosed hypomineralized enamel, providing a more aesthetic appearance.[24](A1)
Other minimally invasive techniques suitable for treating mild to moderate cases of dental fluorosis include enamel microabrasion and resin infiltration. Microabrasion involves mechanically removing the superficial layers of flurosed enamel, thus reducing the visibility of enamel discoloration.[24] This method can have limited effectiveness when treating deeper and more severely discolored lesions.(A1)
The use of dental whitening and microabrasion together has been shown to provide a more aesthetic result and help overcome this limitation. Resin infiltration involves applying hydrochloric acid to etch the enamel, followed by low-viscosity resin, which infiltrates the enamel.[26] Isolation using a rubber dam is recommended.[27] This method has been shown to effectively reduce the visibility of white patches and thus improve cosmesis.[24] (A1)
In cases where these methods are ineffective in improving the appearance of fluorosed teeth, the next minimally invasive step includes using resin-based dental composite bonding to mask the discoloration. This can be in the form of localized fillings or composite veneers. Composite veneers require less, if any, mechanical preparation of the natural tooth and are, therefore, more conservative of tooth structure than traditional veneers.[24] (A1)
In cases with severe discoloration, veneers or conventional crowns may become necessary to achieve a cosmetically acceptable result for the patient. Crowns may be the only viable long-term restorative option in cases with insufficient or poor-quality enamel, as composite and veneer restorations rely on effective enamel-resin bonding for retention.[28](B3)
More invasive indirect restorative options such as veneers and crowns start patients on the restorative cycle leading to the need for lifelong maintenance, patients must be fully informed, and a judgment must be made based on the risks and benefits. Occasionally a combination of the techniques available is required to achieve an optimal aesthetic result.[24](A1)
Differential Diagnosis
The differential diagnoses of dental fluorosis are extensive. They include and are not limited to early carious lesions, molar-incisor hypomineralisation, developmental disorders of enamel and dentine, including amelogenesis imperfecta, Turner hypoplasia, tetracycline staining, and dental manifestations of celiac disease.[29][30][31]
The key to recognizing dental fluorosis is a positive fluoride history within the critical window of amelogenesis, a symmetrical chronological distribution in the pattern of affected teeth, and an increased caries resistance.[22] Clinicians must be able to differentiate dental fluorosis from conditions such as dental caries as the management required varies substantially.[29]
Treatment Planning
Treatment planning is an individualized patient-centered process focusing on prevention and minimally invasive treatment modalities where possible.[26] Once the signs of dental fluorosis are evident in dentition clinically, it is too late for prevention strategies to be effective.[6]
Prevention must be instigated from birth and lies primarily in the education of caregivers and government strategy and policy. These strategies include the control of fluoride levels in drinking water and educating caregivers about the etiology of fluorosis and the importance of receiving the optimum amount of fluoride.[3] This may include avoiding fluoride supplements, especially in areas with fluoridated water, and focusing on the use of topical fluorides such as those in fluoridated toothpaste and mouthwashes.[3]
The primary concern for most patients affected by dental fluorosis is aesthetics.[24] Once patients start on the restorative cycle, they will require lifelong maintenance of their restorations.[32] For this reason, especially where there are minimal symptoms and functional deficits, treatment plans must be centered around the principles of minimally invasive dentistry when possible.[20] Severe cases of dental fluorosis may warrant more destructive therapeutic options, but patients must be fully aware of the risks.[24]
Staging
Multiple indices have been formulated to facilitate the reliable and consistent staging of dental fluorosis.[33] These systems are primarily used in epidemiological studies using clinicians that have been calibrated to increase inter-rater reliability. Indices include the Thylstrup Fejerskov Index, Dean Modified Fluorosis Index, the Tooth Surface Index of Fluorosis, and the Fluorosis Risk Index.[33]
All of these systems are currently in use and are associated with their own strengths and weaknesses.[34] The Dean Modified Index consists of six distinct categories allocating teeth scores ranging from 0 to 5.[34] Its simplicity and ease of use have made it a popular choice amongst epidemiologists and researchers alike.[34][35] However, it has been criticized for its lack of detail where the staging of severe dental fluorosis is concerned.[34]
Table 1. The Dean Modified Fluorosis Index[36]
Code | Description |
0 | Enamel is normal and translucent, glossy, and smooth. |
1 | Enamel is of questionable appearance—neither normal nor warranting a diagnosis of dental fluorosis. There are very slight alterations to the translucency of the enamel, such as opaque white flecks. |
2 | Very mild dental fluorosis with less than 25% of the tooth enamel affected by small opaque white flecks |
3 | Mild dental fluorosis with less than 50% of the tooth enamel affected by opaque white areas |
4 | Moderate dental fluorosis with opaque white areas affecting 50% of the tooth's enamel. There may also be evidence of attrition and dark staining. |
5 | Severe dental fluorosis involves pitting of the dental enamel surface. All surfaces of the tooth are affected. |
The Thylstrup Fejerskov index is an alternative staging system comprised of 10 categories with scores ranging from 0 to 9.[34] It has been described as having biological validity as codes correspond to observable histological enamel changes.[33] The Thylstrup Fejerskov index has significantly more categories relating to severe dental fluorosis.
Table 2.The Thylstrup Fejerskov index[37]
Code | Description |
0 | Normal translucent enamel after air drying tooth surface |
1 | Narrow white lines corresponding to perikymata |
2 | Pronounced lines of opacity following the perikymata with the occasional confluence of adjacent lines. Opacities are less than 2 mm in diameter |
3 | Merging and irregular cloudy areas of opacity. Accentuated drawing of perikymata often visible between opacities |
4 | The entire surface exhibits marked opacity or appears chalky white. Areas exposed to attrition appear less affected. |
5 | The entire surface displays marked opacity with focal loss of outermost enamel (pits) <2 mm in diameter. |
6 | Pits are regularly arranged in horizontal bands <2 mm in vertical extension. Confluent areas <3 mm in diameter exhibit loss of enamel. There is marked attrition |
7 | There is loss of outermost enamel in irregular areas involving <1/2 of the entire surface. Changes in the morphology caused by merging pits and marked attrition |
8 | There is a loss of outermost enamel involving >1/2 of surface |
9 | There is a loss of the main part of the enamel with a change in the anatomic appearance of the surface. A cervical rim of almost unaffected enamel is often noted. |
Prognosis
In mild and moderate cases of dental fluorosis, the prognosis is very good, with concerns and treatment being patient-led with a focus on improving aesthetics and patients being otherwise asymptomatic.[24] Minimally invasive restorative techniques have been shown to be very effective in treating these cases with high levels of patient satisfaction.[26]
In the rarer severe cases of dental fluorosis, the structure of the dentine and enamel becomes compromised.[19] As a result, patients may suffer from dentine hypersensitivity, excessive tooth wear, and enamel fractures. In these cases, minimally invasive techniques produce improvements in appearance.[19]
To produce satisfactory results in more destructive techniques such as full coverage, conventional crowns may need to be considered. If this course is taken, patients must be informed of the lifelong maintenance such restorative work requires, including the need for repair, replacement, and even the eventual loss of teeth.[32]
Complications
In mild and moderate cases of dental fluorosis, the affected dentition is caries resistant.[22] This is unsurprising given the well-documented role of fluoride in caries prevention.[24] In severe cases of dental fluorosis, where the structural integrity of the enamel and dentine are compromised, patients are at a higher risk of dental caries, dentin hypersensitivity, dark discoloration, and tooth wear.[19]
This will impact the aesthetics, function, and longevity of an individual's dentition.[24] Furthermore, it is essential to consider whether patients affected by severe dental fluorosis may also suffer from skeletal fluorosis.[38]
Deterrence and Patient Education
It is important caregivers are informed about the etiology of dental fluorosis and how to avoid it, as dental fluorosis only has the potential to develop during amelogenesis.[39] Such prevention measures include the supervised toothbrushing of children, encouraging children not to ingest dentifrices, and limiting the use of additional fluoride supplements in areas served by fluoridated water.[3]
Patients should also be informed of potentially less publicized sources of fluoride, including tea, artificially fluoridated milk, and fluoridated salt.[3]
The control of fluoride levels within drinking water is vital.[13] This may involve defluoridation techniques where water fluoride levels are excessive. It is equally important to highlight the benefits of fluoridated water and toothpaste in the prevention of dental caries while calling attention to the difference between systemic fluoride administration, which involves ingestion, from topical fluoride administration, which occurs primarily through the use of dentifrices.[39]
Fluoride water concentrations of 0.7-1 ppm are optimal in terms of balancing the beneficial anti-cariogenic properties of fluoride while avoiding complications associated with its excessive ingestion.[13]
Enhancing Healthcare Team Outcomes
Clinically dental fluorosis can be mistaken for a variety of dental conditions.[31] There is no special investigative test in widespread use that easily differentiates dental fluorosis from other conditions with a similar presentation.[21] Instead, diagnosis is contingent on a positive fluoride history during amelogenesis.[21] The incidence of dental fluorosis is increasing, particularly in Europe and the US.[12]
There is a limited window of opportunity for dental fluorosis to develop, starting around birth and ending at approximately eight years of age.[6] For this reason, prevention strategies must be instigated early. Prevention measures encompass a combination of nationally led government strategies to ensure that fluoride concentrations in public drinking water are safe and also professionally led preventative advice to increase public awareness of the benefits of fluoride within a therapeutic range and the risks associated with exceeding it.[39]
Dental professionals and medical professionals, particularly those in contact with expectant mothers and pediatric patients, have a responsibility to inform patients about the risks associated with excessive chronic fluoride intake and provide appropriate advice. A careful balance must be made between the beneficial anti-cariogenic properties of fluoride and the negative effects associated with excessive intake.[3]
Most patients with mild to moderate dental fluorosis are suitable for management by dentists in primary care.[24] Patients with severe dental fluorosis and those requiring complex management will likely require specialist input, which may involve specialists in restorative dentistry, pediatric dentistry, and oral surgeons.[19]
References
Unde MP,Patil RU,Dastoor PP, The Untold Story of Fluoridation: Revisiting the Changing Perspectives. Indian journal of occupational and environmental medicine. 2018 Sep-Dec [PubMed PMID: 30647513]
Level 3 (low-level) evidenceAlmeida LKY,Carvalho TS,Bussaneli DG,Jeremias F, Congenital and acquired defects in enamel of primary teeth: prevalence, severity and risk factors in Brazilian children. European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry. 2021 Aug [PubMed PMID: 33710526]
Aoun A,Darwiche F,Al Hayek S,Doumit J, The Fluoride Debate: The Pros and Cons of Fluoridation. Preventive nutrition and food science. 2018 Sep [PubMed PMID: 30386744]
Yadav KK,Kumar S,Pham QB,Gupta N,Rezania S,Kamyab H,Yadav S,Vymazal J,Kumar V,Tri DQ,Talaiekhozani A,Prasad S,Reece LM,Singh N,Maurya PK,Cho J, Fluoride contamination, health problems and remediation methods in Asian groundwater: A comprehensive review. Ecotoxicology and environmental safety. 2019 Oct 30 [PubMed PMID: 31254856]
Saha A,Mukherjee AK,Ravichandran B, Musculoskeletal problems and fluoride exposure: A cross-sectional study among metal smelting workers. Toxicology and industrial health. 2016 Sep [PubMed PMID: 25653036]
Level 2 (mid-level) evidenceMascarenhas AK, Risk factors for dental fluorosis: a review of the recent literature. Pediatric dentistry. 2000 Jul-Aug; [PubMed PMID: 10969430]
Neurath C,Limeback H,Osmunson B,Connett M,Kanter V,Wells CR, Dental Fluorosis Trends in US Oral Health Surveys: 1986 to 2012. JDR clinical and translational research. 2019 Oct [PubMed PMID: 30931722]
Level 3 (low-level) evidenceKhan ZN,Sabino IT,de Souza Melo CG,Martini T,da Silva Pereira HAB,Buzalaf MAR, Liver Proteome of Mice with Distinct Genetic Susceptibilities to Fluorosis Treated with Different Concentrations of F in the Drinking Water. Biological trace element research. 2019 Jan [PubMed PMID: 29705835]
Wei W,Pang S,Sun D, The pathogenesis of endemic fluorosis: Research progress in the last 5 years. Journal of cellular and molecular medicine. 2019 Apr; [PubMed PMID: 30784186]
DenBesten P,Li W, Chronic fluoride toxicity: dental fluorosis. Monographs in oral science. 2011; [PubMed PMID: 21701193]
Demos LL,Kazda H,Cicuttini FM,Sinclair MI,Fairley CK, Water fluoridation, osteoporosis, fractures--recent developments. Australian dental journal. 2001 Jun; [PubMed PMID: 11491235]
Level 3 (low-level) evidenceMartignon S,Bartlett D,Manton DJ,Martinez-Mier EA,Splieth C,Avila V, Epidemiology of Erosive Tooth Wear, Dental Fluorosis and Molar Incisor Hypomineralization in the American Continent. Caries research. 2021 [PubMed PMID: 33440378]
U.S. Department of Health and Human Services Federal Panel on Community Water Fluoridation., U.S. Public Health Service Recommendation for Fluoride Concentration in Drinking Water for the Prevention of Dental Caries. Public health reports (Washington, D.C. : 1974). 2015 Jul-Aug; [PubMed PMID: 26346489]
Pretty IA,Boothman N,Morris J,MacKay L,Liu Z,McGrady M,Goodwin M, Prevalence and severity of dental fluorosis in four English cities. Community dental health. 2016 Dec; [PubMed PMID: 28537367]
Michel-Crosato E,Biazevic MG,Crosato E, Relationship between dental fluorosis and quality of life: a population based study. Brazilian oral research. 2005 Apr-Jun; [PubMed PMID: 16292450]
Level 3 (low-level) evidenceLevy SM,Hillis SL,Warren JJ,Broffitt BA,Mahbubul Islam AK,Wefel JS,Kanellis MJ, Primary tooth fluorosis and fluoride intake during the first year of life. Community dentistry and oral epidemiology. 2002 Aug [PubMed PMID: 12147170]
DenBesten PK,Yan Y,Featherstone JD,Hilton JF,Smith CE,Li W, Effects of fluoride on rat dental enamel matrix proteinases. Archives of oral biology. 2002 Nov; [PubMed PMID: 12446183]
Level 3 (low-level) evidenceGu LS,Wei X,Ling JQ, [Etiology, diagnosis, prevention and treatment of dental fluorosis]. Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology. 2020 May 9; [PubMed PMID: 32392970]
Level 2 (mid-level) evidenceFarid H,Khan FR, Clinical management of severe fluorosis in an adult. BMJ case reports. 2012 Dec 10 [PubMed PMID: 23230244]
Level 3 (low-level) evidenceOliveira A,Felinto LT,Francisconi-Dos-Rios LF,Moi GP,Nahsan FPS, Dental Bleaching, Microabrasion, and Resin Infiltration: Case Report of Minimally Invasive Treatment of Enamel Hypoplasia. The International journal of prosthodontics. 2020 Jan/Feb; [PubMed PMID: 31860920]
Level 3 (low-level) evidenceArbab Chirani R,Foray H, [Dental fluorosis: etiological diagnosis]. Archives de pediatrie : organe officiel de la Societe francaise de pediatrie. 2005 Mar; [PubMed PMID: 15734125]
Level 3 (low-level) evidenceRevelo-Mejía IA,Hardisson A,Rubio C,Gutiérrez ÁJ,Paz S, Dental Fluorosis: the Risk of Misdiagnosis-a Review. Biological trace element research. 2021 May [PubMed PMID: 32705431]
Kashirtsev F,Tressel J,Simon JC,Fried D, High contrast imaging of dental fluorosis in the short wavelength infrared. Journal of biophotonics. 2021 Oct; [PubMed PMID: 34302430]
Shahroom NSB,Mani G,Ramakrishnan M, Interventions in management of dental fluorosis, an endemic disease: A systematic review. Journal of family medicine and primary care. 2019 Oct [PubMed PMID: 31742127]
Level 1 (high-level) evidenceGreenwall-Cohen J,Greenwall L,Haywood V,Harley K, Tooth whitening for the under-18-year-old patient. British dental journal. 2018 Jul 13; [PubMed PMID: 30002517]
Zotti F,Albertini L,Tomizioli N,Capocasale G,Albanese M, Resin Infiltration in Dental Fluorosis Treatment-1-Year Follow-Up. Medicina (Kaunas, Lithuania). 2020 Dec 29; [PubMed PMID: 33383755]
Pandey P,Ansari AA,Moda P,Yadav M, Enamel microabrasion for aesthetic management of dental fluorosis. BMJ case reports. 2013 Oct 11; [PubMed PMID: 24121810]
Level 3 (low-level) evidenceJhajharia K,Shah HH,Paliwal A,Parikh V,Patel S, Aesthetic Management of Fluoresced Teeth with Ceramic Veneers and Direct Composite Bonding - An Overview and A Case Presentation. Journal of clinical and diagnostic research : JCDR. 2015 Jun [PubMed PMID: 26266231]
Level 3 (low-level) evidenceKashirtsev F,Tressel J,Fried D, Dehydration imaging of dental fluorosis at 1950 nm. Proceedings of SPIE--the International Society for Optical Engineering. 2022 Jan-Feb [PubMed PMID: 35440838]
Alsadat FA,Alamoudi NM,El-Housseiny AA,Felemban OM,Dardeer FM,Saadah OI, Oral and dental manifestations of celiac disease in children: a case-control study. BMC oral health. 2021 Dec 29; [PubMed PMID: 34965875]
Level 2 (mid-level) evidenceMast P,Rodrigueztapia MT,Daeniker L,Krejci I, Understanding MIH: definition, epidemiology, differential diagnosis and new treatment guidelines. European journal of paediatric dentistry. 2013 Sep [PubMed PMID: 24295005]
Level 3 (low-level) evidenceHenry DB, The restorative cycle in dentistry. Today's FDA : official monthly journal of the Florida Dental Association. 2014 Jan-Feb [PubMed PMID: 24707716]
Level 3 (low-level) evidenceRozier RG, Epidemiologic indices for measuring the clinical manifestations of dental fluorosis: overview and critique. Advances in dental research. 1994 Jun; [PubMed PMID: 7993559]
Level 2 (mid-level) evidenceMabelya L,van 't Hof MA,König KG,van Palenstein Helderman WH, Comparison of two indices of dental fluorosis in low, moderate and high fluorosis Tanzanian populations. Community dentistry and oral epidemiology. 1994 Dec; [PubMed PMID: 7882655]
Al Warawreh AM,Al Tamimi ZH,Al Qatawna MI,Al Momani AA,Al Mhaidat MR,El Naji WS,AlSaraireh S, Prevalence of Dental Fluorosis among Southern Jordanian Population. International journal of dentistry. 2020 [PubMed PMID: 33224200]
Public Health Weekly Reports for AUGUST 19, 1938. Public health reports (Washington, D.C. : 1896). 1938 Aug 19 [PubMed PMID: 19315674]
Thylstrup A,Fejerskov O, Clinical appearance of dental fluorosis in permanent teeth in relation to histologic changes. Community dentistry and oral epidemiology. 1978 Nov [PubMed PMID: 282114]
Ramesh M,Malathi N,Ramesh K,Aruna RM,Kuruvilla S, Comparative Evaluation of Dental and Skeletal Fluorosis in an Endemic Fluorosed District, Salem, Tamil Nadu. Journal of pharmacy & bioallied sciences. 2017 Nov [PubMed PMID: 29284943]
Level 2 (mid-level) evidenceBuzalaf MAR, Review of Fluoride Intake and Appropriateness of Current Guidelines. Advances in dental research. 2018 Mar; [PubMed PMID: 29461104]
Level 3 (low-level) evidence