FLUORIDES

IN DENTISTRY

Dr. Eman Almaswary

 Lecture outlines
• INTRODUCTION
• SOURCES OF FLUORIDES
• HISTORY OF FLUORIDES
• METABOLISM OF
FLUORIDES
• MECHANISM OF ACTION
FLUORIDES
• FLUORIDE TOXICITY
• SYSTEMIC FLUORIDES
• TOPICAL FLUORIDES
 PROFESSIONAL
 SELF
 INTRODUCTION
• Fluoride plays an important role in the prevention of dental
caries.
• The cariostatic efficacy of fluorides has been convincingly
demonstrated and the recent decline in caries prevalence is
primarily attributed to the increased use of fluoride agents.

FLUORIDE COMPOSITION
• Fluoride may occur in combined form in a wide variety of
minerals.
 Fluorspar(fluorite CaF2)-49%
 Fluorapatite(Ca10F2(PO4)6 )-3.4%
 Cryolite(Na3ALF6)-54%
• Recognized as the thirteenth most common element in the
earth’s crust
 SOURCE OF FLUORIDE
I. MAIN SOURCES FOR HUMAN EXPOSURE:
• Water
 Seawater at a concentration of around 1.2 – 1.4 mg/litre
 Ground waters at concentrations up to 67 mg/litre
 Surface waters at concentrations less than 0.1 mg/litre
• Fluoride content of rock salt ranges between 40 and 200ppm.
• Food
• It is estimated that the intake of from fish by populations where
fish represents a significant portion of the diet is about
0.5mg/day.
• Fish and seafood products
 Dried seafoods (can contain 290 ppm)
 Canned seafoods (can contain 40 ppm)
SOURCES OF FLUORIDE
 SOURCES OF FLUORIDE
II. Fluoride Rich Dental products
 Fluoridated toothpaste
 Mouth rinse
 Varnish
 Sodium Fluoride tablets
 HISTORY OF FLUORIDES
• In 1805, Morichini found fluoride in human Enamel
• In 1901 Dr. Federick Mckay- “Colorado Stains” minute white
flecks, yellow or brown spots scattered..
• In 1902 Dr. J.M. Eager noticed in Italian emigrants -“denti di
chiaie”
• 1916, Dr. Green supported Mckay’s work with histologic evidence
“an endemic imperfection of the enamel of the tooth”
• In 1918 Dr. O. E. Martin and Mckay- Britton (1898) changed water
supply from shallow wells to deep drilled artesian wells….
• 1931 Mr. H. V. Churchill- spectrographic analysis of Bauxite city
water 13.7ppm
• In 1933, Dr. H. Trendley Dean- conducted “Shoe Leather Survey” in
97 localities, with a aim to find out minimal threshold level…
METABOLISM OF FLUORIDE
 PERMANENT VS. PRIMARY TOOTH

DENTITION PERMANENT PRIMARY

FLUORIDATED 2200PPM 1100PPM

AREAS

NON-FLUORIDATED 950PPM 675PPM

AREAS

• Circulating plasma fluoride is deposited to

 Teeth –
 Dentine contains 4 time more than enamel
 Fluoride concentration in initial stages is more than during completion
 Fluoride concentration in newly erupted teeth is higher in the incisal than
in the cervical margins
 Fluoride concentration in the cementum is higher than any skeletal or
dental tissue
 Bone – 2.6 mg (Remodeling bone deposit more, reversible)
 very small amount to soft tissues
The caries balance. Risk factors and protective factors which shift
the caries balance between de- and remineralization.
 GOALS OF FLUORIDE (F) ADMINISTRATION

1. Do no harm 3. Arrest active decay

Fluorosis or toxicity

2.Prevent decay on intact 4. Remineralize decalcified teeth

dental surfaces

F
 MECHANISM OF ACTION OF FLUORIDE

 The mechanisms by which fluoride increases caries resistance may

arise from both systemic and topical application of fluoride.
1. Increase in the enamel’s resistance to acid solubility
• Enamel formed has more perfect and larger crystals, less solube in
acid, and less likely to develop caries.
• Fluoride favors formation of fluorapatite,
a more acid-resistant apatite than hydroapatite.
2. Increases rat of posteruptive maturation.
3. Remineralization on incipient lesions.
4. Interference with plaque microorganisms.
5. Modification in tooth morphlology
 DEPOSITION OF FLUORHYDROXYAPATITE (FHA) IN
SOUND TOOTH STRUCTURE

 Caries protection results from FHA being more acid resistant

than pure hydroxyapatite (HA)
 Deposition takes place when F replaces hydroxyl groups in HA
 This can occur pre- or post-eruption at neutral pH, or post-
eruptively at neutral or acidic pH
 At low pH, HA dissolves, then re-precipitates as new crystals
which are larger and more acid-resistant due to higher FHA and
lower magnesium and carbonate content
 Deposition of FHA is accomplished both by systemic intake of F
during tooth development, and topical F administration after
eruption
 DEPOSITION

Saliva (S)

Plaque (P)

Tooth (T)
Topical F is the
best method
for deposition.

Increase FHA levels maximally in intact

dental surfaces.
 DEPOSITION OF FLUORIDE

F FHA is more acid resistant than HA

F F
F
F
FHA
Neutral pH

H+ PO4 H+
F
PO4 F FHA
F HA
F CO3
Ca Ca
pH 5.0
Mg
F
H+ Mg and P
CO3 do
FHA H+ not Ca
repreci-
remineralization pitate
 DEPOSITION OF FLUORIDE
Best F uptake is late pre-
Surface eruption and early post-
F build-up eruption
of F

F F F
F F
F

F F F
F
Mature F
enamel

F F Drinking Permanent Primary

Enamel F
F water teeth teeth
fluid
F F
F F 3000 900

Young enamel No F 2000 600

This has better F uptake due Maximal F levels of in outer 5 microns

to more porosity
 BIOAVAILABILITY OF FLUORIDE

 A second theory of caries prevention asserts that Fluoride in

the vicinity of carious activity (in enamel fluid) prevents
dissolution of HA crystals
 Low levels of F (less than 100 ppm to as low as 1ppm), F
must be present when the acid challenge takes place and
therefore must be supplied continually
 A major source of bioavailable Fluoride is residual F in
plaque and pellicle
 Fluoride in plaque minerals such as CaF2 or calculus or in
protein complexes is released during bacterial acid
production.
 BIOAVAILABILITY OF FLUORIDE

Water fluoridation is
an example of a
source.

S F SUGAR

P F ACID

T F

Provide continual low level of F to enamel fluid. The

benefit occurs at the time of decalcification.
 BIOAVAILABILITY OF FLUORIDE

F from plaque
fluid

ACID
F F
F F H+
F F F
F
F F
H+
F
F
F F Protection
from Loosely-bound F
dissolution
will eventually
F Stable FHA become stable

Loosely bound FHA.

F
or adsorbed F

J Arends. JDR
69(SI):601,1990
 BIOAVAILABILITY OF FLUORIDE

H+ F
FHA with no

F
H+ H+ H+
F F H+
F F
PO4
F F F
PO4
F
H+ H+
H+ F Ca
H+ Ca
Protection only H+
where is
F
Incomplete
protection
J Arends. JDR
69(SI):601,1990
 EFFECT ON BACTERIA
FIRST MECHANISM
• At low extracellular pH, fluoride is transported as HF into the
bacterial cell, where it then dissociates into H+ and F–
• This process leads to an accumulation of fluoride inside the cell
and simultaneously to an over-acidification of the cytoplasm
• In the cell, fluoride can inhibit two enzymes: enolase and the
proton releasing adenosine triphosphatase
• Over-acidification of the cytoplasm can also inhibit the
mechanism of glucose transport into the cell
SECOND MECHANISM
• The interference in bacterial adhesion to the tooth’s surface
after pretreatment with fluoridated compounds
 EFFECT ON BACTERIA

F H+ S
S
F
F F
H+ H+
F H+
H+ F
MS
F
H+
F
H+

The presence of fluoride at the time

of glycolytic activity will also
inhibit of plaque acidogenesis.
 SOURCES OF BIOAVAILABLE FLUORIDE

1. saliva
ACT

2. Fluoridated
water 3. Home care products

Topical F 4. RESIDUAL F

F F F F F S
ppm F in saliva
after drinking P
F
0.08 F F F T
0.02
Calcium
Fluoride
1 3 5 h
CaF2 precipitates in plaque during
topical F treatment
 FLUORIDE TOXICITY
PROBABLE TOXIC DOSE (PTD)
• The PTD is 5 mg F/kg body weight
• For a 20 kg, 5 to 6 year old this would be 100 mg and for a 10
kg 2 year old, 50 mg
• Fluoride content of dental products or treatments may
exceed these values for young children.
• For example, a gel tray containing 5 ml of APF contains
61.5mg F
Fluoride is absorbed more quickly when in acidic form
• 100ml of 0.2 or 0.4% F mouthrinse contains 91 or 97mg F
• A tube of fluoridated toothpaste contains as much as 230mg
F.
 SUB-LETHAL TOXIC
 Symptoms are manifested quickly after the dose
 Vomiting
 Excessive salivation
 Tearing and mucous discharge
 Cold wet skin
 Convulsions with higher doses
COUNTER MEASURES
…should be administered immediately…
 emetics, 1% calcium chloride
 calcium gluconate or milk
Calcium reacts with F in the GI tract and prevents its absorption
 The most serious consequences of Fluoride toxicity stem
from reactions of cationic electrolytes with systemic F
 POTENTIAL HARM
Probable toxic dose:
5 mg F / kg body
weight 61.5
mg F/ 91-97 mg
ACT
5 ml F/
container
of F
mouthrinse
Topical F,
12,300 ppm
F pH= 3.5
20 kg 6 year old,
PTD= 100 mg F
Symptoms:
1. Vomiting
2. Excess salivary
and mucous
discharge
230 mg F/
tube 3. Cold wet skin
10 kg 2 year old toothpaste 4. Convulsion at
PTD = 50 mg F higher dose
 POTENTIAL HARM

A serious systemic Counter Measures:

consequence is
binding of F to Ca 1. Emetics
which needed for 2. 1% calcium
heart function. chloride
3. Calcium
F gluconate
4. milk
F F

Ca
F Ca
Divalent
cations like Ca Ca
Ca cause
precipitation,
of F and
F prevent F
Ca Ca F absorbtion in Ca Ca F
F F Ca the intestine. F F Ca
Ca Ca
 FLUOROSIS
• Fluorosis occurs when teeth are developing
• The most critical ages are from 0 to 6 years
• After 8 years, risk of fluorosis is essentially past
• During the critical ages F intake in excess of 0.1mg/kg body
weight/day can lead to fluorosis
• This is roughly 1mg/day for a 1 to 2 year old or 1.5 to 2 mg for a
5 year old
…all forms of F intake comprise the daily consumption…
• This includes water intake (up to 1.5mg/day), foods (0.3 to
1.0mg) and especially significant in young children, swallowed
toothpaste.
• Children under 2 years swallow 50% of toothpaste during tooth
brushing and at 5years, 25%, both of which may amount to
1mg F/day.
 FLUOROSIS

Enamel prism
Excess F affects
mineralization of
developing teeth

Up to age 6 is the critical age for

fluorosis. After age 8, risk is past.
FLUOROSIS

5 year olds swallow

25% of toothpaste Children under 2
years swallow 50%
of toothpaste

1 to 3 grams

Toothpaste = 1 mg
F / gram (1000 “pea” size amount (0.5g) is
ppmF) recommenred for fluorosis
susceptible children.
 mild moderate

pitting severe
 DELIVERY OF FLUORIDES

COMMUNITY BASED INDIVIDUAL METHODS

SYSTEMIC TOPICAL

PROFESSIONALLY APPLIED
WATER FLUORIDATION FLUORIDE VARNISH
FLUORIDE TABLETS GEL/FOAM
MILK FLUORIDATION SELF APPLIED
SALT FLUORIDATION TOOTHPASTE
MOUTHRINSE , ETC
 FLUORIDE SUPPLEMENTS

AGE <0.3ppm 0.3-0.6ppm >0.6ppm

0-6m 0 0 0

6m-3y 0.25 mg 0 0

3-6y 0.5 mg 0.25 mg 0

6-16y 1.0 mg 0.5 mg 0

DIETARY FLUORIDE SUPPLEMENTAL SCHEDULE

Academy of Pediatric Dentistry current recommendations

 WATER
FLUORIDATION

1945
Grand Rapids
Michigan

1948: Grand Rapids had 60% less DMFT than Muskegon ‘control’ city

Optimal level: 0.7 - 1.2 ppm F

Colder climates drink less water need higher fluoride level
• The Department of Health and Human Services recently has proposed to not
have a fluoride range, but rather to limit the recommendation to the lower
limit of 0.7 ppm F
• Rationale is to balance the benefits of preventing dental caries while reducing
the chance of fluorosis [AAPD GUIDELINE ON FLUORIDE THERAPY, 2014]
 SCHOOL WATER
FLUORIDATION

BENEFITS
• Suitable alternative
• Fluoride consumed during • Both pre eruptive and post
school days eruptive effects
• Topical effect through
• 4.5 to 6.3 ppm-
release in saliva
• No fluorosis • Least expensive and most
• Caries reduction 45 to 50% effective
• “Halo effect” or “Diffusion”
Feasibility
 FLUORIDE VARNISH
• Application of F varnish is essentially a professional topical F
treatment
• Commercially Available - Duraflor is currently the only
concentrated F varnish sold in the US (called Duraphat in Europe)
and contains 5% NaF
• Fluor Protector contains 0.7% silane F and is used as a cavity
varnish.
• For topical treatments
 Duraflor should be applied to, and allowed to dry on all cotton roll-
isolated teeth
 Afterwards the patient should not eat for 2 hours
 Although the caries benefits are similar to topical F gels, less total F
is released into the oral cavity during treatment (i.e., only 3 to 6mg
) than from gels.
 INDICATIONS
• Apply to teeth during operating room procedures
 Enamel incipiencies
 Exposed roots
 Margins of restorations
 Teeth at risk which cannot be sealed such as erupting
molars or premolars
 Carious anterior teeth in very young children
 FLUORIDE VARNISH

Duraflor – 5% NaF,
26,000 ppm F, 3-6 mg F
per dose.

Fluor-Protector – 0.7%
silane F. Used as a cavity
varnish
 HOME RINSES

• These are available as over-the-counter (OTC) daily rinses

(0.05% NaF, 230 ppm F; 0.02% NaF, 200 ppm)
• As prescription weekly rinses (0.2% NaF, 910ppm F or 0.4%
SnF2, 970ppm F)
• Patients should rinse ONCE/day for 1 minute with 10ml.
INDICATIONS
 High caries risk patients
 Exposed root surfaces
 School prevention programs
 HOME FLUORIDE RINSES
Daily Rinse: Weekly Rinse

0.2% NaF, 0.091% free

ACT F, 910 ppm F, 9.1 mg F /
dose.
PREVI-
DENT
0.05% NaF, 0.023%
free F, 230 ppm F, 2.3
mg F / dose

Indications:
1. High caries risk
2. Exposed roots
PHOS 3. Prevention programs
-FLOR

0.02% APF, 0.02%

free F, 200 ppm F, 2
mg F / dose.
 HOME GELS

• Home gels are available as prescription 1.1% NaF (5000ppm F)

and 0.4% SnF2 (1000ppm)
• These are self-administered by the exposure of fluoride to
teeth than do rinses.
INDICATIONS
 High or severe (rampant) caries risk patients
 Exposed root surfaces when evidence of caries is present
 School prevention programs
 HOME GELS

GEL-CAM – Indications:

0.4% SnF2, 1. Severe caries

0,097% free F, 2. Root caries
970 ppm F, 2- 3. Prevention
3mg programs
F/ dose.

PREVIDENT –
1.1% NaF,
0.5% free F,
5000 ppm, 10-
25 mg F/ dose.
Radiation
caries
 DENTIFRICES
• Dentifrices are sold as pastes or gels
• Gel theoretically penetrates retention sites better, and are more
acceptable to young children than pastes
• Fluoride salts commonly used are:
 0.2% NaF
 0.76% sodium monofluorophosphate (MFP)
 0.4% SnF2
• Most dentifrices contain 1mg F/gram which amounts to 1mg or
1000ppm F in each tooth-brushing dose
• A few newer products contain up to 1500ppm F
• The main ingredients of dentifrices, from a preventive
standpoint, are Fluoride salts and abrasives
• According to trial data, all F dentifrices reduce caries by 25 to
32% versus control paste without F, when used twice daily
DENTIFRICE (TOOTHPASTE)

Pastes
Key ingredients in TP:
1. F salt
2. Abrasive

Gels
1. Better interdental penetration
2. More acceptable to children
 DENTIFRICES
USE CONSIDERATIONS
• Noteworthy concerns are fluorosis from swallowed toothpaste in
children and the F content of commercial products
• Accepted provisions for reducing child intake of fluoride are use of
toothbrushes with small heads to limit paste application
• A ‘smear’ or ‘rice-size’ amount of fluoridated toothpaste
(approximately 0.1 mg fluoride) should be used for children less
than three years of age
• A ‘pea-size’ amount of fluoridated toothpaste (approximately 0.25
mg fluoride) is appropriate for children aged three to six
..high concentration F dentifrice should not be used before age 7..
• Parents should dispense the toothpaste and perform or assist
with tooth brushing of preschool-aged children
 ….should you rinse after tooth-brushing???….
• To maximize the beneficial effect of fluoride in the toothpaste,
rinsing after brushing should be kept to a minimum or eliminated
altogether
• Finally, tooth-brushing should be conducted just before bed-time
in order to take advantage of night-time reduction of oral
clearance mechanisms.
• F bioavailability will thus be increased

‘Smear’ – under 3 yrs ‘Pea-sized’ – 3 to 6 yrs

 FLUORIDE USE CONSIDERATIONS

S F
High
P
salivary
T flow

F awake

Brush before
S
F F F
bedtime
F P F Low
salivary
F T
F F F flow

asleep
F
Evidence shows that
increased F use and F Rinsing after brushing
concentration increases reduces F effectiveness by
bioavailability in 50%.
stagnation sites.
Recommendations: Do not
(Note: be aware of rinse after brushing or rinse
fluorosis susceptible with a F rinse.
patients.)
any questions