| Dental fluorosis |
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Mild fluorosis: in its usual mildest form, fluorosis appears as opaque white patches on the enamel
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| Classification and external resources |
| ICD-10 |
K00.3 |
| ICD-9-CM |
520.3 |
Dental fluorosis (also termed mottled enamel)[1] is hypomineralization of tooth enamel caused by ingestion of excessive fluoride during enamel formation.[2]
It appears as a range of visual changes in enamel[3] causing degrees of intrinsic tooth discoloration. The severity of the condition is dependent on the dose, duration and age of the indiviudal during the exposure.[1] In the mildest form (which is the most common) there are faint white lines or specks. Slightly more severe cases appear as white mottled patches, while severe fluorosis is characterized by brown discoloration and brittle, pitted and rough enamel.
Barring the most severe cases, teeth with fluorosis are relatively resistant to dental caries (tooth decay),[4] although they may be of potential cosmetic concern.[4]
Contents
- 1 Classification
- 1.1 Dean's index
- 1.2 TF index
- 2 Causes
- 3 Mechanism
- 4 Management
- 5 Diagnosis
- 6 Epidemiology
- 7 History
- 8 References
Classification
Severe fluorosis: brown discolored and mottled enamel of an individual from a region with high levels of naturally occurring fluoride
Severe fluorosis: the enamel is pitted and discolored
The 2 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.[5]
Dean's index
Dean's fluorosis index was first published in 1934. The index underwent two changes, appearing in its final form in 1942.[6] An individual's fluorosis score is based on the most severe form of fluorosis found on two or more teeth.[7]
Dean's Index
| 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. It scores the spectrum of fluorotic changes in enamel from 0 to 9, allowing more precise definition of mild and severe cases.[5]
Causes
The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). These changes are prone to occur in children who are excessively exposed to fluoride between 20 and 30 months of age. The critical period of exposure is between 1 and 4 years old, and the child is no longer at risk after 8 years of age (apart from the wisdom teeth).[8] 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.[9] Individual susceptibility to fluorosis is also influenced by genetic factors.[8]
Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), 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.[10] 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.[10][11] Severe cases can be caused by exposure to water that is naturally fluoridated to levels well above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.[12]
Mechanism
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.[5][4] Fluoride may also indirectly alter the action of protease via a decrease in the availability of free calcium ions in the mineralization environment.[5] 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.[4]
Traditionally severe fluorosis has been described as enamel hypoplasia, however hypoplasia does not occur as a result of fluorosis.[5] 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.[5]
Hydroxyapatite is converted to fluorohydroxyapatite as follows:
Ca10(PO4)6(OH)2 + F-- + H+ → Ca10(PO4)6(OH)F + H2O
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:
- Tooth bleaching
- Micro-abrasion
- Composite fillings
- Veneers
- Crowns
Generally more conservative options such as bleaching are sufficient for mild cases.
Diagnosis
Amelogenesis imperfecta: this condition can be mistaken for fluorosis
The differential diagnosis for this condition includes:
- Turner's hypoplasia (although this is usually more localized)
- Some mild forms of amelogenesis imperfecta
- Enamel defects caused by infection of a primary tooth predecessor
The teeth may have to be dried to detect fluorosis.[7]
Epidemiology
As of 2005[update] surveys conducted by the National Institute of Dental and Craniofacial Research in the USA between 1986 and 1987[13] and by the Center of Disease Control between 1999 and 2002[14] are the only national sources of data concerning the prevalence of dental fluorosis.
NIDR and CDC findings on children
| Deans Index |
1987 |
2002 |
| Questionable fluorosis |
17% |
11.8% |
| Very mild fluorosis |
19.85% |
| Mild fluorosis |
4% |
5.83% |
| Moderate fluorosis |
1% |
2.71% |
| Severe fluorosis |
0.3% |
| Total mild cases |
17% |
15.83% |
| Total severe cases |
0.65% |
2.71% |
| Total |
5.57% |
10.05% |
The U.S. Centers for Disease Control found a 9% higher prevalence of dental fluorosis in a 1999-2002 study of American children than was found in a similar survey from 1986-1987. 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] It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million), and in children who have a poor intake of calcium.[citation needed]
Dietary reference intakes for fluoride[13]: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.
Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit.
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 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."[15]
History
In ancient times, Galen describes what is thought to be dental fluorosis.[5] 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.[16] He writes that the condition is called "Denti di Chiaie" (Chiaie teeth), named after Stefano Chiaie, an Italian professor.[16] 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".[5] 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."[5] 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.[5] Gradually, they became aware of existing and further reports of a similar condition worldwide.[5]
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.[17][18][19][20] The condition then started to become termed "dental fluorosis".[20] Through epidemiological studies in the USA, Henry Trendley Dean helped to identify a causal link between high concentrations of fluoride in the drinking water and mottled enamel.[5] He also produced a classification system for dental fluorosis that is still used in modern times, Dean's Index.[5] As research continued, the protective effect of fluoride against dental decay was demonstrated.[5]
References
- ^ a b Dean JA (10 August 2015). McDonald and Avery's Dentistry for the Child and Adolescent (10th ed.). Elsevier Health Sciences. p. 132. ISBN 978-0-323-28746-3.
- ^ Wong, MC; Glenny, AM; Tsang, BW; Lo, EC; Worthington, HV; Marinho, VC (20 January 2010). "Topical fluoride as a cause of dental fluorosis in children.". The Cochrane database of systematic reviews (1): CD007693. PMID 20091645.
- ^ Bergc JH; Slayton RL (26 October 2015). Early Childhood Oral Health. John Wiley & Sons. p. 113. ISBN 978-1-118-79210-0.
- ^ a b c d Neville BW; Chi AC; Damm DD; Allen CM (13 May 2015). Oral and Maxillofacial Pathology (4th ed.). Elsevier Health Sciences. pp. 52–54. ISBN 978-1-4557-7052-6.
- ^ a b c d e f g h i j k l m n Fejerskov O; Kidd E (16 March 2009). Dental Caries: The Disease and Its Clinical Management. John Wiley & Sons. pp. 299–327. ISBN 978-1-4443-0928-7.
- ^ Meiers P. "HT Dean´s epidemiology of Mottled Teeth". The History of Fluorine, Fluoride and Fluoridation. Retrieved 12 November 2015.
- ^ a b Whelton H, Browne D, Felicia P, Whelton J. "E-training for Dean’s Index Version 2". Oral Health Services Research Centre, University College Cork, Ireland. Retrieved 12 November 2015.
- ^ a b Clark, MB; Slayton, RL; Section on Oral, Health (September 2014). "Fluoride use in caries prevention in the primary care setting.". Pediatrics 134 (3): 626–33. PMID 25157014.
- ^ Alvarez JA, Rezende KMPC, Marocho SMS, Alves FBT, Celiberti P, Ciamponi AL (2009). "Dental fluorosis: exposure, prevention and management" (PDF). Med Oral Patol Oral Cir Bucal 14 (2): E103–7. PMID 19179949.
- ^ a b United States Environmental Protection Agency (2010). "Comment-Response Summary Report for the Peer Review of the Fluoride: Dose-Response Analysis for Non-Cancer Effects Document". Lay summary (PDF) – EPA (2010).
- ^ Yeung CA (2008). "A systematic review of the efficacy and safety of fluoridation". Evid Based Dent 9 (2): 39–43. doi:10.1038/sj.ebd.6400578. PMID 18584000. Lay summary (PDF) – NHMRC (2007).
- ^ Fawell J, Bailey K, Chilton J, Dahi E, Fewtrell L, Magara Y (2006). "Environmental occurrence, geochemistry and exposure". Fluoride in Drinking-water (PDF). World Health Organization. pp. 5–27. ISBN 92-4-156319-2. Retrieved 2009-01-24.
- ^ a b Fluoridation Facts (PDF). American Dental Association. 2005. p. 29. Archived from the original (PDF) on March 7, 2007.
- ^ "Table 23, Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999--2002". Centers for Disease Control and Prevention. 2005. Retrieved 2006-10-29.
- ^ Frequently Asked Questions (FAQ), American Dental Association Website accessed February 4, 2012
- ^ a b Eager JM (November 1, 1901). "Denti di Chiaie (Chiaie teeth)". Public Health Reports 16 (44): 2576–2577. PMC 1438998. PMID 818673.
- ^ Velu H; Balozet L (1931). "Reproduction experimentale chex Iemouton de la dystrophie dentaire des animaux des zones phosphates". Bull Acad Vet France 4: 373.
- ^ Churchill HV (1931). "Occurrence of fluorides in some water of the United States". Ind Eng Chern 23: 996.
- ^ Smith, MC; Lantz, EM; Smith, HV (4 September 1931). "The cause of mottled enamel.". Science (New York, N.Y.) 74 (1914): 244. PMID 17755565.
- ^ a b Teotia, SP (1999). "Dental fluorosis." (PDF). The National medical journal of India 12 (3): 96–8. PMID 10492579.
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Oral and maxillofacial pathology (K00–K06, K11–K14, 520–525, 527–529)
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Lips
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- Cheilitis
- Actinic
- Angular
- Plasma cell
- Cleft lip
- Congenital lip pit
- Eclabium
- Herpes labialis
- Macrocheilia
- Microcheilia
- Nasolabial cyst
- Sun poisoning
- Trumpeter's wart
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Tongue
|
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- Ankyloglossia
- Black hairy tongue
- Caviar tongue
- Crenated tongue
- Cunnilingus tongue
- Fissured tongue
- Foliate papillitis
- Glossitis
- Geographic tongue
- Median rhomboid glossitis
- Transient lingual papillitis
- Glossoptosis
- Hypoglossia
- Lingual thyroid
- Macroglossia
- Microglossia
- Rhabdomyoma
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Palate
|
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- Bednar's aphthae
- Cleft palate
- High-arched palate
- Palatal cysts of the newborn
- Inflammatory papillary hyperplasia
- Stomatitis nicotina
- Torus palatinus
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Oral mucosa - Lining of mouth
|
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- Amalgam tattoo
- Angina bullosa haemorrhagica
- Behçet syndrome
- Bohn's nodules
- Burning mouth syndrome
- Candidiasis
- Condyloma acuminatum
- Darier's disease
- Epulis fissuratum
- Erythema multiforme
- Erythroplakia
- Fibroma
- Focal epithelial hyperplasia
- Fordyce spots
- Hairy leukoplakia
- Hand, foot and mouth disease
- Hereditary benign intraepithelial dyskeratosis
- Herpangina
- Herpes zoster
- Intraoral dental sinus
- Leukoedema
- Leukoplakia
- Lichen planus
- Linea alba
- Lupus erythematosus
- Melanocytic nevus
- Melanocytic oral lesion
- Molluscum contagiosum
- Morsicatio buccarum
- Oral cancer
- Benign: Squamous cell papilloma
- Keratoacanthoma
- Malignant: Adenosquamous carcinoma
- Basaloid squamous carcinoma
- Mucosal melanoma
- Spindle cell carcinoma
- Squamous cell carcinoma
- Verrucous carcinoma
- Oral florid papillomatosis
- Oral melanosis
- Pemphigoid
- Pemphigus
- Plasmoacanthoma
- Stomatitis
- Aphthous
- Denture-related
- Herpetic
- Smokeless tobacco keratosis
- Submucous fibrosis
- Ulceration
- Verruca vulgaris
- Verruciform xanthoma
- White sponge nevus
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Teeth (pulp, dentin, enamel)
|
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- Amelogenesis imperfecta
- Ankylosis
- Anodontia
- Caries
- Concrescence
- Delayed eruption
- Dens evaginatus
- Dentin dysplasia
- Dentin hypersensitivity
- Dentinogenesis imperfecta
- Dilaceration
- Discoloration
- Ectopic enamel
- Enamel hypocalcification
- Enamel hypoplasia
- Enamel pearl
- Fluorosis
- Fusion
- Gemination
- Hyperdontia
- Hypodontia
- Maxillary lateral incisor agenesis
- Impaction
- Macrodontia
- Meth mouth
- Microdontia
- Odontogenic tumors
- Keratocystic odontogenic tumour
- Odontoma
- Open contact
- Premature eruption
- Pulp calcification
- Pulp canal obliteration
- Pulp necrosis
- Pulp polyp
- Pulpitis
- Regional odontodysplasia
- Resorption
- Shovel-shaped incisors
- Supernumerary root
- Taurodontism
- Trauma
- Avulsion
- Cracked tooth syndrome
- Vertical root fracture
- Occlusal
- Tooth loss
- Tooth wear
- Abrasion
- Abfraction
- Acid erosion
- Attrition
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Periodontium (gingiva, Periodontal ligament, cementum, alveolus) - Gums and tooth-supporting structures
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- Cementicle
- Cementoblastoma
- Cementoma
- Eruption cyst
- Epulis
- Pyogenic granuloma
- Congenital epulis
- Gingival enlargement
- Gingival cyst of the adult
- Gingival cyst of the newborn
- Gingivitis
- Desquamative
- Granulomatous
- Plasma cell
- Hereditary gingival fibromatosis
- Hypercementosis
- Hypocementosis
- Linear gingival erythema
- Necrotizing periodontal diseases
- Acute necrotizing ulcerative gingivitis
- Pericoronitis
- Peri-implantitis
- Periodontal abscess
- Periodontal trauma
- Periodontitis
- Aggressive
- As a manifestation of systemic disease
- Chronic
- Perio-endo lesion
- Teething
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Periapaical, mandibular and maxillary hard tissues - Bones of jaws
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- Agnathia
- Alveolar osteitis
- Buccal exostosis
- Cherubism
- Idiopathic osteosclerosis
- Mandibular fracture
- Microgenia
- Micrognathia
- Intraosseous cysts
- Odontogenic: periapical
- Dentigerous
- Buccal bifurcation
- Lateral periodontal
- Globulomaxillary
- Calcifying odontogenic
- Glandular odontogenic
- Non-odontogenic: Nasopalatine duct
- Median mandibular
- Median palatal
- Traumatic bone
- Osteoma
- Osteomyelitis
- Osteonecrosis
- Bisphosphonate-associated
- Neuralgia-inducing cavitational osteonecrosis
- Osteoradionecrosis
- Osteoporotic bone marrow defect
- Paget's disease of bone
- Periapical abscess
- Periapical periodontitis
- Stafne defect
- Torus mandibularis
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Temporomandibular joints, muscles of mastication and malocclusions - Jaw joints, chewing muscles and bite abnormalities
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- Bruxism
- Condylar resorption
- Mandibular dislocation
- Malocclusion
- Crossbite
- Open bite
- Overbite
- Overjet
- Prognathia
- Retrognathia
- Temporomandibular joint dysfunction
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Salivary glands
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|
- Benign lymphoepithelial lesion
- Ectopic salivary gland tissue
- Frey's syndrome
- HIV salivary gland disease
- Necrotizing sialometaplasia
- Mucocele
- Pneumoparotitis
- Salivary duct stricture
- Salivary gland aplasia
- Salivary gland atresia
- Salivary gland diverticulum
- Salivary gland fistula
- Salivary gland hyperplasia
- Salivary gland hypoplasia
- Salivary gland neoplasms
- Benign: Basal cell adenoma
- Canalicular adenoma
- Ductal papilloma
- Monomorphic adenoma
- Myoepithelioma
- Oncocytoma
- Papillary cystadenoma lymphomatosum
- Pleomorphic adenoma
- Sebaceous adenoma
- Malignant: Acinic cell carcinoma
- Adenocarcinoma
- Adenoid cystic carcinoma
- Carcinoma ex pleomorphic adenoma
- Lymphoma
- Mucoepidermoid carcinoma
- Sclerosing polycystic adenosis
- Sialadenitis
- Parotitis
- Chronic sclerosing sialadenitis
- Sialectasis
- Sialocele
- Sialodochitis
- Sialosis
- Sialolithiasis
- Sjögren's syndrome
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Orofacial soft tissues - Soft tissues around the mouth
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- Actinomycosis
- Angioedema
- Basal cell carcinoma
- Cutaneous sinus of dental origin
- Cystic hygroma
- Gnathophyma
- Ludwig's angina
- Macrostomia
- Melkersson–Rosenthal syndrome
- Microstomia
- Noma
- Oral Crohn's disease
- Orofacial granulomatosis
- Perioral dermatitis
- Pyostomatitis vegetans
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Other
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- Eagle syndrome
- Hemifacial hypertrophy
- Facial hemiatrophy
- Oral manifestations of systemic disease
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Index of the mouth
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| Description |
|
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| Disease |
- Congenital
- face and neck
- cleft
- digestive system
- Neoplasms and cancer
- Other
- Symptoms and signs
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| Treatment |
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