“What is Dental Fluorosis?”
©1996 - 2004 PFPC
Dental fluorosis is an enamel defect caused by an excessive intake of fluorides during the time of enamel formation.
Depending on the time of exposure and the amount of fluoride (“peak amounts”) sections of the forming tooth may become either hypomineralized or hypermineralized (Appleton et al, 2000; Rajan et al, 1989, Susheela et al, 1999; Lyaruu et al, 1987; Martignon & Valbuena, 1998; Pergolizzi et al, 1995; ten Cate et al, 1998; etc.).
This results in mottling of the tooth which shows up initially as “white spots”, progressing into permanently stained, brown mottled teeth.
The enamel in turn now beomes subject to decay, thus leading to the formation of caries, lesions or cavities.
The tooth becomes more porous, with porosity of the tooth affected increasing relative to the degree of fluorosis.
The degree of fluorosis is directly related to tooth eruption.
The more fluoride is taken in, the longer it takes for the tooth to erupt. The later a tooth erupts, the more severe the fluorosis.
As dental fluorosis can only occur during the stage of enamel formation it is seen by all sides as the first visible sign that an overdose of fluoride has occurred in the child during this vulnerable period.
While in other countries the first mottled tooth is seen as sign of fluoride poisoning, dental fluorosis is proclaimed to be a mere “harmless cosmetic defect” by Western dental health organizations, and public health agencies such as the US CDC.
A recent three-year study conducted in Sosnivka, Ukraine investigated the health of children afflicted with dental fluorosis and compared results to children without such enamel defects, the only such study we know of. It was found that children with dental fluorosis had more gastrointestinal diseases (37%), respiratory diseases (29.5%), bone and muscle diseases (13.8), mental disorders (11.3), skin diseases (9.4%), and 8.2% suffered from diseases of the nervous system and sensory dysfunction. As children grew older, there was also in increase in urino-genital diseases. Boys suffered more from mental, bone-muscle, and birth anomalies. The girls had more sight problems and vaginal veneral disease. In all tested groups boys were shorther than the control. In addition children with dental fluorosis had much higher caries occurrence (Miroshnychenko, 2000).
The dental profession states that the biochemical events which lead to dental fluorosis are still unknown (Gerlach et al, 2000;Limeback, 1994;Wright et al, 1996).
Identical enamel defects were observed in iodine-deficient areas already more than 80 years ago (McKay, 1918), making it clear that this enamel condition is brought upon by thyroid dysfunction (aberrant G-protein signalling) during the time of enamel formation. The fact that the severity of fluorosis is directly correlated to eruption of teeth, is a further sign of the implication, as since at least the 1930s has it been known that thyroid hormones control tooth eruption.
The enamel defects in dental fluorosis resemble those of “Amelogenesis Imperfecta” (Winter, 1996).
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Aoki H - “Ultrastructural changes induced in rat ameloblasts and enamel by NaF administration, especially the stages of transition and maturation” Shikwa Gakuho 89(10):1605-37 (1989)
“Changes in the enamel: In the forming enamel, a calciotraumatic line consisting of hypermineralized and hypomineralized layers could be seen. Another hypermineralized line appeared at the enamel surface adjacent to the transitional stage.”
Appleton J - “Dentinogenesis and the calciotraumatic response to the injection of lead or fluoride ions” Scanning Microsc 6(4):1073-80 (1992)
“With fluoride, there was formation of a hypermineralized band succeeded by a relatively hypomineralized band...”
Appleton J, Chestersa J, Kierdorf U , Kierdorf H - "Changes in the
Structure of Dentine from Cheek Teeth of Deer Chronically Exposed to High Levels of Environmental Fluoride" Cells Tissues Organs 167:266-272 (2000)
"The primary and secondary dentine was characterised by the presence of interglobular dentine and regular bands of hypo- and hypermineralised dentine." (Appletona et al., 2000)
Gerlach RF, de Souza AP, Cury JA, Line SR - “Fluoride effect on the activity of enamel matrix proteinases in vitro” Eur J Oral Sci 108(1):48-53 (2000)
Larsen MJ, Thorsen A - “A comparison of some effects of fluoride on apatite formation in vitro and in vivo” Calcif Tissue Int 36(6):690-6 (1984)
“Corresponding to the plasma fluoride peak and the decrease of plasma calcium, a hypermineralized layer was formed while a hypomineralized zone was formed during plasma calcium increase after disappearance of fluoride.”
Li YJ, Zhao BR, Yao B, Ge LH, Yao JX, Shi GS - “The characters on histopathological changes in dental fluorosis” Shanghai Kou Qiang Yi Xue 2(4):218-20 (1993)
- “...the future of the lesion is enamel-hypoplasia,enamel rods were hypomineralized...the space among enamel rods widen and form some cavities.”
Lyaruu DM, de Jong M, Bronckers AL, Woltgens JH - “Ultrastructure of in-vitro recovery of mineralization capacity of fluorotic enamel matrix in hamster tooth germs pre-exposed to fluoride in organ culture during the secretory phase of amelogenesis.” Arch Oral Biol 32(2):107-15 (1987)
Limeback H - “Enamel formation and the effects of fluoride” Community Dent Oral Epidemiol 22(3):144-7 (1994)
Martignon S , Valbuena F - "Prevalence of developmental enamel defects in first permanent molars and incisors in children aged 5-9 years attending public and private schools" ABSTRACTS from 2nd EADPH Congress, September 25-26, 1998, Santander, Spain, Originally Published in Community Dental Health Volume 15 Number 3 (1998)
- "Diffuse hypermineralization was observed most (61.1%) which is related in the literature to the chronic ingestion of fluoride. The prevalence of white/cream localised hypomineralization was 33.2%. Hypoplasia was seen in only 0.7%." (Martignon & Valbuena, 1998)
Miroshnychenko O - Sosnivka Final Report, Ecoprava Liev, under USAid Scientific Assessment Grant (2000)
Pergolizzi S, Santoro A, Santoro G, Trimarchi F, Anastasi G - “Enamel fluorosis in rat's incisor: S.E.M. and T.E.M. investigation” Bull Group Int Rech Sci Stomatol Odontol 38(3-4):95-104 (1995)
Rajan BP, Gnanasundaram N, Santhini R - “Serum and urine fluoride levels in toothpaste users” J Indian Dent Assoc 59(6,7,8,9):137-42 (1987)
Rajan BP, Gnanasundaram N - Report by Ministry of Environment and Forest, Government of India, 1989.
Susheela AK, Bhatnagar M, Gnanasundram N, Saraswathy TR - “Structural aberrations in fluorosed human teeth: Biochemical and scanning electron microscopic studies”
ten Cate JM, Damen JJ, Buijs MJ - “Inhibition of dentin demineralization by fluoride in vitro” Caries Res 32(2):141-7 (1998)
- “...This leads to the formation of a surface layer, which may even be hypermineralized compared to sound dentin.”
UCLA - What is Caries?
Winter GB - “Amelogenesis imperfecta with enamel opacities and taurodontism: an alternative diagnosis for 'idiopathic dental fluorosis'.” Br Dent J 181(5):167-72 (1996)
Woltgens JH, Lyaruu DM, Bronckers AL, Bervoets TJ, Van Duin M - “Biomineralization during early stages of the developing tooth in vitro with special reference to secretory stage of amelogenesis” Int J Dev Biol 39(1):203-12 (1995)
“Many of the fluoride-induced changes in the enamel organ are reversible: young ameloblasts recover and resume secretion and mineralization of the fluorotic matrix when fluoride is removed from the medium. This recovery is enhanced when medium calcium levels are increased. Only the changes in the hypermineralized enamel remain irreversible. Thus, we hypothesize that fluoride induces a local hypocalcemia in the enamel fluid surrounding the enamel crystals by stimulating a hypermineralization of the pre-existing enamel crystals.”
Wright JT, Chen SC, Hall KI, Yamauchi M, Bawden JW - “Protein characterization of fluorosed human enamel” J Dent Res 75(12):1936-41 (1996)