Dental fluorosis A concise presentation for under graduate students of dentistry.

1. Presented by
Dr Aurlene, MDS
Senior Lecturer
Department of Public Health Dentistry
Madha Dental College and Hospital

2. DENTAL FLUOROSIS
 Fluoride is often denoted as ‘a double edged sword’
 Dental fluorosis occurs as a result of excess fluoride ingestion during tooth
formation.
 Enamel fluorosis can only occur when teeth are forming, and therefore
fluoride exposure (as it relates to dental fluorosis) occurs during childhood.

3. CONTENTS
 Introduction
 Epidemiology of fluorosis in India
 Etiology of dental fluorosis
 Pathology and pathogenesis of dental fluorosis
 Clinical features of dental fluorosis
 Measurement of dental fluorosis
 Prevention of dental fluorosis
 Treatment of dental fluorosis

4. Introduction
 Definition: “Hypoplasia or hypomineralisation of tooth enamel or dentine
produced by the chronic ingestion of excessive amounts of fluoride during the
period when teeth are developing.”
 The optimal daily fluoride intake has been estimated to be 0.06 mg/kg body
weight by the US Environmental Protection Agency.
 Ingestion of water with a fluoride concentration two or three times greater than
the recommended amount causes mild dental fluorosis, whereas water containing
four times the recommended amount causes severe dental fluorosis.
 Teeth are most susceptible to fluorosis when they are in the early maturation
stage of enamel development
 As different teeth develop at different times and individual teeth themselves
develop in incremental stages, the period of maximum susceptibility to fluorosis is
different for different teeth.
 The permanent teeth (except the third molars) are considered collectively to be
susceptible to development of fluorosis during the first 6–8 years of life.

5. EPIDEMIOLOGY OF FLUOROSIS IN INDIA
National Oral Health Survey and Fluoride Mapping
2002-2003
Prevalence of dental fluorosis
12 years – 12.1 %
15 years – 11.8 %
In India, high levels of fluoride are reported in
around 230 districts in 20 states.
The total population at risk for fluorosis is around
11.7 million as of 2014.

6. ETIOLOGY
NATURAL SOURCES
 Fluoride exposure from natural sources such as ground water. In areas with
high fluoride in ground water, fluoride gets concentrated in vegetables, fruits,
tea and other crops.
 High levels of fluoride in atmosphere is present in areas of volcanic activity.
 High levels of fluoride are also found naturally in foods such as canned fish
particularly salmon and sardines, jowar, banana, potatoes, yams, cassava,
rock salt and tea.

7. ETIOLOGY
ARTIFICIAL SOURCES
 Industrial exposure due to fluoride released into the environment (coal
burning, welding, power generation, production of steel, iron, aluminum,
zinc, phosphorus, chemical fertilizers, bricks, glass, plastic, cement, and
hydrofluoric acid.
 Fluoride mouthrinses, fluoride tooth pastes, fluoride gels, fluoridated salt,
fluoridated milk, fluoridated water.
 Fluoride containing drugs such as benzothiazidines used as diuretics,
anesthetics such as enflurane and methoxyflurane.

8. PATHOLOGY
Sub-surface porosity in the enamel along with alternating bands of hypo
and hyper mineralization within the forming enamel.

9. AMELOGENESIS AND BIOMINERALISATION
 Four stages in tooth enamel development;
 PRE-SECRETORY – Pre-ameloblasts differentiate into ameloblasts
 SECRETORY – Ameloblasts secrete enamel matrix proteins and lay down a thin layer of
aprismatic enamel close to mantle dentin. Tome’s process forms and lays down prismatic
(rod) and interprismatic (interred) enamel. Matrix protein amelogenin is secreted into
enamel space. At the end of this stage, ameloblasts lose their Tome’s process and a final
layer of aprismatic enamel is laid down.
 TRANSITION – Enamel matrix proteins undergo rapid proteolysis leaving a porous enamel
matrix
 MATURATION – Matrix proteins removed from extracellular space and mineralization
increases to form fully mineralized enamel matrix.

11. PATHOGENESIS (DELAY IN REMOVAL OF
PROTEIN MATRIX)
 Decreases proteinase activity (Matrix metalloproteinase 20, kallikrein 4)
thereby leading to retention of amelogenin and delay in final mineralization.
 Fluoride incorporated into enamel crystal enhances binding of amelogenin
and inhibits growth of the crystal
 Large amount of protons released during formation of hydroxyapatite
combine with fluoride to form hydrofluoric acid (HF)
 HF in the cytoplasm of ameloblast causes stress and decreases synthesis of
KLK 4.

12. Source: CASTIBLANCO RUBIO GA, MARTIGNON S, CASTELLANOS PARRA JE, NARANJO M, ALFONSO W. Pathogenesis of dental fluorosis: biochemical
and cellular mechanisms. Revista Facultad de Odontología Universidad de Antioquia. 2017 Jun;28(2):408-21.

13. Clinical Features
 Dental fluorosis usually occurs symmetrically within dental arches, the most
commonly affected tooth is the premolar followed by the second molar,
maxillary incisor, canine, first molar and mandibular incisors.
 MILD CASES - white opaque appearance of the enamel, many thin white
horizontal lines running across the surfaces of the teeth, with white opacities
at the newly erupted incisal end.

14. Clinical Features
 In moderate cases of fluorosis, there is marked opacity and
the entire tooth can appear chalky white. The deeper layers
of the enamel are affected and teeth can erupt with pits.
Yellow to light brown staining in areas of enamel damage are
also a hallmark of moderate fluorosis.
 In very severe cases, the enamel is porous, poorly
mineralized, stains brown, and contains relatively less
mineral and more proteins than sound enamel. Severely
fluorosed enamel can easily chip post eruptively during
normal mechanical use.

16. Measurement of dental fluorosis
 The most commonly used index for measuring fluorosis is the Dean’s fluorosis
index, originally introduced in 1934 by Trendley H Dean and then modified in
1942.

17. Prevention of dental fluorosis
INDIVIDUAL LEVEL
 Following recommended dietary allowance for daily fluoride intake 0.06 mg/kg body
weight
 Use of fluoride free toothpaste upto the age of 2 years
 Use only a pea size amount of fluoride toothpaste for children between 3 – 6 years
of age.
 Instruct children to spit and not swallow tooth paste after brushing. Supervise while
children are brushing.
 Restrict use of fluoride supplements, and other professionally applied topical
fluorides in fluoride endemic areas.
 Calcium rich diet
COMMUNITY LEVEL
 Defluoridation of water supplies
 Changing to an alternative source of water
 Nutritional interventions
 The NPPCF (National Program for Prevention and Control of Fluorosis) has been
introduced in India in 2008 to tackle fluorosis in the country.

18. TREATMENT OF DENTAL FLUOROSIS
 The treatment option varies according to the severity of dental fluorosis
Microabrasion
Bleaching
Composite restorations
Veneers
Full crowns

19. BLEACHING
In-office vital bleaching using McInnes solution.
Source: Sherwood IA. Fluorosis varied treatment options. Journal of conservative dentistry: JCD. 2010 Jan;13(1):47.

20. MICROABRASION
 Teeth are abraded using water cooled fine diamond finishing flame shaped
points, with diamond abrasive particle size of 20 - 30μm with a high speed
hand piece to remove surface enamel layer of 0.5mm thickness. Final
polishing of teeth is done with polishing discs.
Source: Sherwood IA. Fluorosis varied treatment options. Journal of conservative dentistry: JCD. 2010 Jan;13(1):47.

21. COMPOSITE RESTORATION
Source: Sherwood IA. Fluorosis varied treatment options. Journal of conservative dentistry: JCD. 2010 Jan;13(1):47.

22. Full mouth rehabilitation using PFM
crowns
Source: Sherwood IA. Fluorosis varied treatment options. Journal of conservative dentistry: JCD. 2010 Jan;13(1):47.