Fluoride and its Implications on Oral Health: A Review

ABSTRACT

This article aims to review the literature about the history of fluoride, its toxicity, prevalence, prevention, diagnosis, and management in oral healthcare practice. Fluoride is the cornerstone of oral health, playing a pivotal role in oral health. Fluoride can be administered topically or systemically. Topically, it is found in toothpaste, mouth rinses, and professional treatments such as fluoride varnish. These directly shield teeth from decay and strengthen the existing enamel. Systemically, fluoride is ingested through water, foods, or supplements, benefiting tooth development, especially in children. Nevertheless, responsible fluoride use is essential. Overexposure can lead to dental fluorosis, affecting tooth aesthetics. Consulting a dentist for personalized guidance on fluoride usage can help strike the right balance between oral protection and potential side effects, ensuring a radiant and healthy smile for life.

INTRODUCTION

Fluoride in the environment and its relationship to human health is quite extensive and spans a wide variety of disciplines including the fields of medicine, dentistry, environmental and occupational health, toxicology, environmental geology, petrology, geochemistry, economic geology, hydrogeology, and soil science.[1]

Fluoride in the natural environment is very uneven; largely a result of the geochemical behavior of this element (fluorine) that is preferentially enriched in highly evolved magmas and hydrothermal solutions, which explains why high concentrations are often found in syenites, granitoid plutonic rocks, alkaline volcanics, and hydrothermal deposits. Fluoride can also occur in sedimentary formations that contain fluoride-bearing minerals derived from the parent rock, fluoride-rich clays, or fluorapatite.[1]

Dissolved fluoride levels are usually controlled by the solubility of fluorite (CaF₂); thus, high concentrations are often associated with soft, alkaline, and calcium-deficient waters.

Fluoride enters the body with food, through respiration, and products containing fluoride. Fluoride is a part of the natural environment and is therefore constantly present in people’s lives. However, the concentration of fluoride can vary from one region to another.[2]

Oral healthcare is fundamental for any individual’s health. Dental caries is still one of the major public health problems. The most effective way of caries prevention is the use of fluoride for remineralization of tooth’s enamel layer.[3]

Minerals are lost (demineralization) from a tooth’s enamel layer when acids formed from plaque bacteria and sugars in the mouth, which attack the enamel.

History

Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs. When he arrived, McKay was astounded to find scores of Colorado Springs natives with grotesque brown stains on their teeth.

McKay’s first big break came in 1909, when renowned dental researcher Dr. G.V. Black agreed to come to Colorado Springs and collaborate with him on the mysterious ailment.

The Colorado Springs Dental Society conducted a study showing that almost 90% of the city’s locally born children had signs of brown stains. When Black arrived in the city, he too was shocked by the prevalence of Colorado Brown Stain in the mouths of native-born residents.[4]

Dr. H. Trendley Dean, head of the Dental Hygiene Unit at the National Institute of Health (NIH) began investigating the epidemiology of fluorosis. By the late 1930s, he and his staff had made a critical discovery, namely fluoride levels of up to 1.0 ppm (parts per million) in drinking water did not cause enamel fluorosis in most people, and only mild enamel fluorosis in a small percentage of people was observed.

As research continued, it was subsequently recognized that the ingestion of fluoride in optimal amounts provided protection against the development of dental caries without staining the teeth (Dean, 1938). Based on these findings and additional studies conducted during the 1940s, it was suggested that public drinking water supplies in the US be fluoridated with an optimal level of 0.7 to 1.2 mg/L, depending on the ambient air temperature of the region.[4]

Etiology and Pathogenesis: H. Trendley Dean and Elias Evolve in 1936 identified the association between increased fluoride intake and mottled enamel.

The mechanism of fluorosis has been related to the alteration of enamel mineralization caused by a delay in the removal of amelogenesis at the early-maturation stage of enamel formation.[5]

The severity of fluorosis is highly dependent on fluoride dose, exposure, duration, and the age of the child.[6]

The risk of fluoride overexposure occurs between the ages of 3 months and 8 years and the critical period for susceptibility to enamel fluorosis varies between males and females.[7]

Prevalence

Dental fluorosis is prevalent in many areas of Asia and Africa where the ground water contains a higher concentration of fluoride. More than 23 countries in the world are endemic fluoride areas, in which approximately 100 million people are suffering from dental fluorosis; it has been shown that 40% of the population appears to have developmental enamel defects and around 20% have fluorosis characterized by diffused opacities that are mainly mild.[8]

The World Health Organization (WHO) has set the upper limit of fluoride concentration in drinking water at 1.5 mg/L and the Bureau of Indian Standards, has therefore, laid down Indian standards as 1.0 mg/L as the maximum permissible limit of fluoride with further remarks as “lesser the better.” Intake of fluoride higher than the optimum level is associated with dental and skeletal fluorosis.[9]

In India, fluoride was first detected in drinking water at the Nellore district of Andhra Pradesh in 1937 (Ayoob and Gupta, 2006). Since then, considerable work has been done in different parts of India to explore the fluoride-laden water sources [Table 1].[10]

Table 1.

Prevalence of fluoride in India

State	District	Range
Assam	Goalpara, Kamrup, Karbi Anglong, and Nagaon	1.45-7.8
Andhra Pradesh	Adilabad, Anantpur, Chittoor, Guntur, Hyderabad, Karimnagar, Khammam, Krishna, Kurnool, Mahbubnagar, Medak, and Nalgonda	1.8-8.4
Bihar	Aurangbad, Banka, Buxar, Jamui, Kaimur (Bhabua), Munger, Nawada, Rohtas, and Supaul	1.7-2.8
Chhattisgarh	Baster, Bilaspur, Dantewada, Janjgir-Champa, Jashpur, Kanker, Korba, Koriya, Mahasamund, Raipur, Rajnandgaon, and Surguja	1.5-2.7
Delhi	North West Delhi, South Delhi, South West Delhi, Kanjhwala, Najafgarh, East Delhi	1.57-6.1
Gujarat	Ahmedabad, Amreli, Anand, Banaskantha, Bharuch, Bhawnagar, Dohad, Junagarh, Kachchh, Mehsana, Narmada, Panchmahals, Pantan, Rajkot, Sabarkantha, Surat	1.6-6.8
Haryana	Bhiwani, Faridabad, Gurgaon, Hisar, Jhajhar, Jind, Kaithal, Kurushetra, Mahendergarh, Panipat, Rewari, Rohtak, Sirsa and Sonipath	1.5-17
Jammu and Kashmir	Doda, Rajouri, and Udhampur	2.0-4.21
Karnataka	Bagalkot, Bengaluru, Belgaon, Bellary, Bidar, Bijapur, Chamarajanagar, Chikmagalur, Chitradurga, Davangere, Dharwad, Gadag, Gulburga, Haveri, Kolar, Koppal, Mandya, Mysore, Raichur, Tumkur	1.5-4.4
Kerala	Palakkad, Palghat, Allepy, Vamanapuram, and Alappuzha	2.5-5.7
Maharashtra	Amravati, Chandrapur, Dhule, Gadchiroli, Gondia, Jalna, Nagpur, Nanded	1.51-4.1
Madhya Pradesh	Bhind, Chhattarpur, Chhindwara, Datia, Dewas, Dhar, Guna, Gwalior, Harda, Jabalpur, Jhabua, Khargaon, Mandsaur, Rajgarh, Satna, Seoni, Shajapur, Sheopur, and Sidhi	1.5-10.7
Orissa	Angul, Balasore, Bargarh, Bhadrak, Bandh, Cuttack, Deogarh, Dhenkanal, Jejpur, Keonjhar, and Sonapur	1.52-5.2
Punjab	Amritsar, Bhatinda, Faridkot, Fatehgarh Sahib, Firozpur, Gurdaspur, Mansa, Moga, Muktsar, Patiala, and Sangrur	0.44-6.0
Rajasthan	Ajmer, Alwar, Banaswara, Barmer, Bharatpur, Bhilwada, Bikaner, Bundi, Chittaurgarh, Chura, Dausa, Dhaulpur, Dungarpur, Ganganagar, Hanumangarh, Jaipur, Jaisalmer, Jalor, Jhunjhunu, Jodhpur, Karaoli, Kota, Nagaur, Pali, Rajsamand, Sirohi, Sikar, Sawai Madhopur, Tonk, and Udaipur	1.54-11.3
Tamil Nadu	Coimbatore, Dharmapuri, Dindigul, Erode, Karur, Krishnagiri, Namakkal, Perambalur, Puddukotai, Ramanathapuram, Salem, Sivaganga, Theni, Thiruvannamalai, Tiruchirappalli, Vellore, and Virudhunagar	1.5-3.8
Uttar Pradesh	Agra, Aligarh, Etah, Firozabad, Jaunpur, Kannauj, Mahamayanagar, Mainpuri, Mathura, and Mau	1.5-3.11
West Bengal	Bankura, Bardhaman, Birbhum, Dakshin Jaipur, Malda, Nadia, Purulia, Uttar Dinajpur	1.5-3.8

Fluoride toxicity

Fluoride toxicity is a condition in which there are elevated levels of the fluoride ion in the body. The American Dental Association has recommended that no more than 120 mg fluoride (264 mg sodium fluoride) be dispensed at any one time.[11]

Acute toxicity

Most cases of acute fluoride toxicity have followed accidental ingestion of sodium fluoride. Large cases of fluoride exposure are due to the ingestion of dental fluoride products.

Chronic toxicity

In India, an estimated 60 million people have been poisoned by well water contaminated by excessive fluoride, which is dissolved from the granite rocks. The effects are particularly evident in the bone deformities of children. Similar or larger problems are anticipated in other countries including China, Uzbekistan, and Ethiopia.

Common signs and symptoms of fluoride toxicity include nausea, vomiting, and a drop in blood calcium, causing local or general signs of muscle tetany.

Methods of minimizing toxicity

Weekly rinsing with 0.2% NaF mouth rinse (1 mg/mL F) will not produce toxicity. However, ingestion of 50 mL of the same mouth rinse will lead to toxicity.

Studies have indicated that stannous fluoride preparations are slightly more toxic than sodium fluoride or sodium monoflurophosphate preparations. Based on reports analyzed by Dukes (1980) and Bayless and Tinanoff (1985), it was concluded that the probable toxic dose (PTD) of fluoride for children is 5.0 mg F/kg.

Clinical features and classifications

Mild fluorosis is often unnoticeable, and the enamel contains small areas of white lines or brown spot.

Clinical image of mild fluorosis in a patient in the Department of Dental and Maxillofacial Surgery, Lady Hardinge Medical College and Hospital Figure 1a.

Figure 1.

(a) Clinical image of mild fluorosis in a patient in the Department of Dental and Maxillofacial Surgery, Lady Hardinge Medical College and Hospital, (b) Clinical image of severe fluorosis in a patient in the Department of Dental and Maxillofacial Surgery, Lady Hardinge Medical College and Hospital, (c) Indirect porcelain veneering performed in a severe fluorosis case

Severe fluorosis, in contrast, can exhibit diffuse opaque mottling and brown discoloration of the enamel with a rough and pitted surface. The brown or black discoloration occurs after the eruption of the tooth due to potential internalized extrinsic staining of the porous enamel.

Clinical image of severe fluorosis in a patient in the Department of Dental and Maxillofacial Surgery, Lady Hardinge Medical College and Hospital is shown in Figure 1b.

Classification systems for fluorosis

Two of the most widely used fluorosis indices are:

• Dean’s Index, (1934) which is based on the extent and severity of the enamel defects appearance: normal, questionable, very mild, mild, moderate, and severe fluorosis.[12]

• Thylstrup and Fejerskov Index (TFI) 1978, which is based on the biological aspects and clinical appearance and includes scores from 0 (normal enamel) to 9 (severe fluorosis).[12]

Diagnosis

The differential diagnosis for dental fluorosis includes:

1. Mild forms of amelogenesis imperfecta (AI) (mainly hypomaturation type).

2. Early decalcified carious lesions.

3. Molar, incisor hypomineralization (MIH), and other environmental enamel defects and localized enamel hypoplasia due to trauma or infection of the primary teeth (Turner’s hypoplasia).[13]

The diagnosis of fluorosis depends on taking an accurate and detailed history and undertaking a thorough clinical and radiographic examination.

Management

Tooth bleaching, enamel micro abrasion, enamel macro abrasion, conservative direct composite restorations, or indirect porcelain veneers are commonly used for the management of enamel opacities, depending on the severity of the defects.[14]

Mild fluorosis can be treated with conservative options such as vital bleaching and enamel micro abrasion.[15]

A combination of enamel micro abrasion and bleaching has been shown to be more effective than micro abrasion alone in aesthetic management of teeth with fluorosis.[16]

Macro abrasion involves the use of fine-grit water-cooled diamond abrasives or multi-fluted finishing burs on a high-speed handpiece, lightly swept over the stained area for 5-10 s to remove the hypomineralized enamel. Macro abrasion is indicated for the management of enamel defects greater than 0.1-0.3 mm that are not amenable to treatment using conservative micro abrasion techniques.[17]

An initial enamel biopsy using a high-speed diamond bur would be a helpful technique to estimate the depth of the enamel opacities and determine the appropriate treatment modality.

For more severe fluorosis, direct composite restoration or indirect porcelain veneers may be considered as suitable options in adult patients [Figure 1c].

Bleaching of discolored teeth before the placement of restorations may be indicated in severely discolored cases to reduce the need for the removal of significant amounts of tooth tissue.

CONCLUSION

Fluoride occurs naturally in our environment and is always present in our lives. Exposure can occur through dietary intake, respiration, and fluoride supplements. Fluoride can be toxic in extremely high concentrations.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.