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Preventive Dentistry (Lecture 9) Other caries preventive factors Fluoride I Dr. Caroline Mohamed

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Preventive Dentistry. (Lecture 9) Other caries preventive factors Fluoride I Dr. Caroline Mohamed. Outline of lectures. OTHER CARIES-PREVENTIVE FACTORS Fluorides Occurrence and intake Toxicology - PowerPoint PPT Presentation

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Page 1: Preventive Dentistry

Preventive Dentistry(Lecture 9)

Other caries preventive factorsFluoride I

Dr. Caroline Mohamed

Page 2: Preventive Dentistry

Outline of lectures

OTHER CARIES-PREVENTIVE FACTORS Fluorides

Occurrence and intake

Toxicology

Pre-eruptive effect of fluoride on tooth

formation

Post-eruptive effects of fluoride

Arrest of caries

Remineralization

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FLUORIDES•Fluorides have unique external modifying effects on caries initiation and progression.

However, a prerequisite for optimal effect is a combination of excellent mechanical and chemical plaque control, targeting the cause of dental caries-the cariogenic plaque.

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•We should use fluoride in populations and individuals with:

– a high prevalence of caries, – poor standards of oral hygiene, and – no exposure to fluoride,

a restriction in frequency of intake of sticky, sugar-containing products would result in some decrease in caries incidence. •Salivary stimulation is an important caries-preventive measure in caries-susceptible patients who have a reduced salivary flow.

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Occurrence and intake

 

•Halogen•Compound form of fluorine.•A trace element- computer analyses.•Very reactive gas.•Not found in free elemental form in nature.•Major source is from water – artesian wells.•Found in soils rich in fluorspar, cryolite, and other minerals.•In biologic materials, the concentration of fluoride is generally as low as a few parts per million or less.

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•Soil..( 0.05 to 190 mg/m3)•Food… ( 0.2 to 1 ppm or more )•Drugs•Fertilizers ..( ..42.000 mg/kg)•The most important fluoride-containing minerals are fluorspar CaF2, and fluorapatite which are widespread in many countries.

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• Normally the fluoride concentration in

groundwater is limited to 0.2 to 2.0 ppm, but, for example in the United States, India and some African countries, fluoride concentrations greater than 60.0 ppm have been reported.

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By contrast, most surface water contain less than 0.1 ppm of fluoride.

In rivers, it may range from 0.1 to 1.0 ppm of fluoride.

Seawater contains 1.2 to 1.4 ppm of fluoride.

Concentrations may be altered locally by undersea volcanic activity.

Most fluoride in water exists as free fluoride ions.

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Dietary sources - drinking water

• Waterborne fluorides are the most important source of flouride for humans.

• Modern diets as a source of flouride.• Use of fluoridated water in preparation of processed

foods and beverages. Hallo effect.• For temperate climates

– Optimal fluoride level: 1 ppm of fluoride.

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Dietary sources - foods

• Fluoride in foods.– Nonfluoridated communities: 1 mg/day.– Fluoridated communities: 2 – 3 mg/day.

• Not known to be a significant factor in fluorosis (mottled enamel).

• Small amounts: fruits, vegetables, cereals.

• Rich amounts: seafoods and tea leaves.

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Dietary sources - drinking water

• For infants and young children– Intake of 2 – 4 glasses of water: 0.5 – 1 mg of

fluoride.

• For older children, adolescents and adults– Intake of 6 – 8 glasses of water: 1.5 – 2 mg of

fluoride.

• Ingestion of fluoride greater than optimal levels in drinking water (2 ppm) may cause fluorosis.

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•Mineral water may contain 1.8 to 5.8 mg of fluoride/L.

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Dietary sources - foodsTable 1. Fluoride Concentration in Fresh Foods and Beverages

Food Range of F in ppm

Beer 0.15 – 0.86

Cereals 0.18 – 2.8

Citrus fruits 0.07 – 0.17

Coca Cola 0.07

CoffeeInstant (powder)

0.2 – 1.61.7

Fish without bone or skin 1.0

Fish meal 80.0 – 250.0

Milk 0.04 – 0.55

Noncitrus fruits 0.03 – 0.84

Sardines 8.0 – 40.0

Shrimp meat 0.4

Shrimp shell 18.0 – 48.0

TeaInstant (solution)

Leaves

0.1 – 2.00.2

75 – 110

Vegetables and tubers 0.02 – 0.9D Caroline Mohamed 13

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•Tea leaves are a particularly rich source of fluoride, most of which is rapidly released into tea infusions, within 5 to 10 minutes. •The fluoride concentrations of brewed tea commonly range from 0.5 to 4.0 ppm.

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•Fluoride intake from diet(including drinking water and beverages with less than 6.0 mg of F/L) and recommended use of fluoride-containing dental products such as toothpastes, mouthrinses, lozenges, and chewing gums will normally have no adverse effect on general health in young adults and adults.•However, up to the age of 6 years, it is well known that a high intake of fluoride will result in visible fluorosis of the teeth.

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Early use of fluoride tooth paste

• Young children in whom the swallowing reflex is not fully developed can ingest up to 0.3 –o,5mg F at each brushing.

• The risk is not as high as fluoride supplement

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• Infant formula: Because its own F content and especially because it is mixed with fluoridated water.

• Other factors that have been associated with susceptibility of populations to dental fluorosis are altitude, renal insufficiency, and possibly malnutrition.

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Metabolism - absorption

• Major site of absorption: stomach.

• Studies with animals suggest intestinal absorption also occurs.

• Soluble fluoride in drinking water is 100% completely absorbed, whereas 50 – 80% of the fluoride in foods is absorbed.

• Oral mucosa can absorb fluoride in small quantities.

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Metabolism - Distribution

• Teeth and skeleton have the highest concentrations of fluoride.– Due to the affinity of fluoride to calcium.– Cementum, bone, dentin, and enamel.

• Fluoride content of teeth increases rapidly during early mineralization periods and continues to increase with age, but at a slower rate.

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Metabolism - Excretion• Principal route of excretion is urine (90 –

95%).

• Remaining 5 – 10% in the feces.

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Metabolism - Excretion• Directly related to the degree of active bone

growth.• Fluoride excretion is lower when a child is

growing rapidly and is actively depositing bone material than in adults with a mature bone structure and fully mineralized teeth.

• About half of the ingested fluoride is excreted in the urine each day.

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Metabolism - storage

• Deposited in calcified structures.

• Skeletons of older persons contain more fluoride than those of younger ones.– Amount of fluoride in bone gradually

increases with age– Greatest during active growth years.

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Metabolism - storage

• Factors that attract fluoride to bones:1. Presence of an active growth area at the

ends of long bones.

2. Small size of the bone crystals.

3. Close contact between bones and the blood supply

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Metabolism - storage

• Deposited in the enamel through diffusion.– Carious enamel may take up 10 times more

fluoride than adjacent healthy enamel to inhibit expansion of carious lesion.

• Dentin may contain even more fluoride.– Chemically similar to bone– Highest concentration found adjacent to pulp:

close to blood supply.

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Relative safety• Low and moderate intake results to

( related to general health and age ):– Skeletal fluorosis– Mottled enamel– Osteosclerosis (hardening of bone)– Exostoses (bony projections) ( linked to

impaired renal function)– Calcification of ligaments

• High intake may result to death.

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•The intake of fluoride associated with the development of enamel fluorosis of the permanent teeth has been estimated to range from 40 to 100 μg/kg of body weight per day. •Infants consuming formulas made from concentrated liquids, or powders diluted with water providing 1,000 μg of fluoride/L, are at risk of dental fluorosis (1000 µg/L=1 mg/L). •The fluoride-concentration will increase when water is boiled in Teflon-coated vessels.

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•The maturation phase of the maxillary incisors occurs at 22 to 26 months of age ( around 2 years of age), when susceptibility to fluorosis is greatest. •For the incisors, fluoride exposure prior to this period ( < 2 years of age ) carries less risk than exposure for up to 36 months ( around 5 years age ) subsequently; a period corresponding to the maturation phase of the incisors (approximately 2-3 years old).

•The clinical implications are the central and lateral incisors are susceptible to fluorosis as a result of excessive fluoride intake up to age 5 years, with peak susceptibility at around the age of 2 years.

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•To prevent the development of visible and esthetically disturbing fluorosis, fluoride intake in infants and preschool children should therefore be limited and controlled.

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Permanent Teeth Calcification Begins (Months) Eruption (Years)

Maxilla     Central incisor 3-4 7-8

Lateral incisor 10- 12 8-9

Canine 4-5 11-12

First premolar 8-21 10-11

Second premolar 24-27 10-12

First molar 0-1 5-6

Second molar 30-36 12-13

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•The risk for and severity of fluorosis are closely correlated with the plasma fluoride level during enamel maturation. •The later in life enamel mineralization occurs, the more severe the enamel fluorosis is likely to be, even assuming a constant dose of fluoride from birth. •The pattern of fluorosis in the permanent dentition is strongly correlated to the time of maturation of the tooth enamel for the homologous pairs of teeth.

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Severe fluorosis

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Skeletal fluorosis

Mottled enamel

Exostoses

osteosclerosis

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Mottled enamel (Endemic Dental

Fluoride)• White or brown spotty staining of tooth enamel.

– May be due to food, debris, or plaque.• Sometimes will have horizontal striations.• Enamel is deficient in:

1.Number of cells producing enamel causes pitting (hypoplasia).

2.Hypocalcification causes chalkiness.

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Mottled enamel (Endemic Dental

Fluoride)• Occurs only in teeth that are being formed.

– The risk of developing fluorosis is strongly correlated to the regular intake of fluoride during tooth mineralization, particularly during the maturation phase of the enamel.

– When exposed to high concentrations of fluoride, opaque spots will develop on the enamel.

• High intake of fluoride results to mottled enamel.

• Protection of fluoride is decreased by severe fluorosis.

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Dean (1936) suggested classification of the dentition into one of seven categories, according to the degree of enamel changes (fluorosis), from 0 for normal enamel to 7 for severe fluorosis. Scores from 1 to 6 comprised the stages questionable, very mild, mild, moderate, and moderately severe.

Later Dean (1942) combined moderately severe and severe into one score, namely severe to include all enamel surfaces with any type of surface destruction, irrespective of degree.

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Criteria for Dean's Fluorosis IndexScore Criteria

Normal The enamel represents the usual translucent semivitriform type of structure. The surface is smooth, glossy, and usually of a pale creamy white color.

Questionable The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to occasional white spots. This classification is utilized in those instances where a definite diagnosis of the mildest form of fluorosis is not warranted and a classification of "normal" is not justified.

Very Mild Small opaque, paper white areas scattered irregularly over the tooth but not involving as much as 25% of the tooth surface. Frequently included in this classification are teeth showing no more than about 1-2 mm of white opacity at the tip of the summit of the cusps of the bicuspids or second molars.

Mild The white opaque areas in the enamel of the teeth are more extensive but do not involve as much as 50% of the tooth.

Moderate All enamel surfaces of the teeth are affected, and the surfaces subject to attrition show wear. Brown stain is frequently a disfiguring feature.

Severe Includes teeth formerly classified as "moderately severe and severe." 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.

Source: Dean, 1942. As Reproduced in "Health Effects of Ingested Fluoride" National Academy of Sciences, 1993. pp. 169.

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Mottled enamel (Endemic Dental

Fluoride)

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Toxicology •Topical fluoride agents are safe and harmless if used strictly as directed.•The probable toxic dose defined as the threshold dose that could cause serious or life threatening systemic signs and symptoms necessitating immediate emergency treatment and hospitalization, is 5 mg of F/kg of body weight.•Child death is likely to occur if a child ingests a fluoride dose in excess of 15 mg of F/kg of body weight.•A dose as low as 5 mg of F/kg body weight may be fatal for some children.

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•It is essential that the fluoride concentrations in dental products be known to the persons who use them. •It is even more important to know the amount of fluoride contained in standard packaging (bottles of tablets, tubes of toothpaste, etc) as well as the amounts involved during routine usage and how these amounts relate to the probable toxic dose.

 

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Symptoms of acute toxicity•Fluoride toxicity is characterized by a variety of signs and symptoms. •Symptom onset usually occurs within minutes of exposure. •Severity of symptoms can depend on the amount of fluoride ingested/ age/weight/health condition of the patient.

• Symtoms:GastrointestinalAbdominal painDiarrhea Dysphagia HypersalivationMucosal injury NauseaVomiting

Electrolyte abnormalitiesHyperkalemia Hypocalcemia Hypoglycemia Hypomagnesemia

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Neurological effectsHeadache Hyperactive reflexes Muscle weakness Muscular spasmParesthesiaSeizures Tetanic contractions Tremor

CardiovascularCardiac arrest Shock Various arrhythmias

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Method of action (fluoride toxicity)Ingested fluoride initially acts locally on the intestinal mucosa.

It can form hydrofluoric acid in the stomach, which leads to gastrointestinal irritation or corrosion.

After ingestion, the gastrointestinal tract is the earliest and most commonly affected organ system.

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Treatment

In case of accidental swallowing, give milk, calcium carbonate or milk of magnesia to slow absorption.

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Mechanisms of anticaries action of fluoride

1. Increase in the enamel’s resistance to acid solubility

• Enamel formed has more perfect and larger crystals, less soluble in acid, and less likely to develop caries.

• Fluoride favors formation of fluorapatite, a

more acid – resistant apatite than

hydroxyapatite.

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Mechanisms of anticaries action of fluoride

2. Remineralization• Greater concentration of fluoride released from

the dissolved enamel or already present on the

plaque, the more will remineralization be

favored and carious process be slowed.

• Use of topical fluoride raises the fluoride level of

tooth surface and underlying tissues to a level

expected to protect against caries.

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Mechanisms of anticaries action of fluoride

3. Antibacterial effects of fluoride− Inhibition of enzymes essential to cell

metabolism and growth.− Lower the surface energy of the tooth.− Can strip off bacteria from hydroxyapatite.− Fluoride can bind more effectively to positively

charged areas on the apatite crystal than can the bacteria.

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Systemic Theory of fluoride action

• Pre-eruptive fase• Systemic fluoride during teeth mineralization leads to F

enamel absortion ( fluorapatita) and more resistance to decay.

• May enhance the resistance of the tooth by way of:

1. An alteration in tooth morphology, ( cusps are rounder , the fissures are more shallow, fissure approximation is abrupt and tight and

2. A conversion of the hydroxiapatite mineral to fluoridated state with an attendant reduction in solubility and an enhancement of the mineralization phase of the caries process

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Pre-eruptive fase and post-eruptive fase.•In teeth, as in all the mineralized tissues, fluoride levels tend to be greatest at the surface nearest the tissue fluid that supplies the fluoride. •Pre eruptive accumulation is highest on the pulpal aspect of the dentin and the outer surface of the enamel. •A much higher total fluoride concentration is found in the dentin because of endogenous fluoride supply from the vessels of pulp. •The outer surface of the enamel will receive a "topical” supply of fluoride from the surrounding follicular fluid, explaining why fluoride concentrations decrease from the inner surface of the dentin and the outer surface of the enamel, respectively.

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•The concentration of fluoride is also higher in those parts of the enamel that are the first to develop and mature ie, the incisal edges of the anterior teeth and the occlusal surfaces of the molars and premolars. •These pre eruptive effects of fluoride may reduce susceptibility to initiation of fissure caries in the molars during eruption and possibly around the approximal contact surfaces before secondary, posteruptive maturation is completed.

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Post eruptive

• After tooth formation fluoride is no longer involved systemically in tooth formation. However consumed fluoride is excreted through the saliva and can aid in tooth protection throughout the life.

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Post eruptive effects• Providing fluoride only before eruption does not

afford maximum protection against caries.• Thus topical mechanisms are considered important

in caries prevention independent of systemic fluorides.

• The post eruptive beneficial effect of fluoride likely occurs primarily from the presence of fluoride in the fluid phase at the tooth surface.

• Fluoride is responsible for decreasing demineralization when the tooth is exposed to organic acids and for increasing the rate for remineralization

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•Post eruptive accumulation has an important fase during eruption of the molars, a critical period for the initiation of fissure caries, because of the extremely high plaque reaccumulation rate, until the teeth reach occlusion.

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•Fluoride accumulates in the plaque fluid as CaF2,on the enamel surface. During the acid challenge, CaF2 is dissolved.•The enamel surface; acts as a ‘micropore filter’ and Fˉ and H + ions (HF) diffuse into the subsurface lesion, increasing the amounts of fluoride in the active lesion compared to the surrounding intact enamel. •Within the lesion, the F- ions retard demineralization of the enamel crystals during the acid challenge and enhance remineralization by crystal growth and accumulalion of fluorapatite (FA) on the crystal surfaces when the pH rises.

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•Hite spots caries lesions can successfully be arrested if the patient maintains a high standard of approximal plaque control and applies fluoride toothpaste.

•The total amount of fluoride is increased in the arrested lesion.•At the subclinical, microscopic level, repeated cycles or acid challenge, followed by pH rise, combined with frequent (daily) access to low concentrations of fluoride from water and toothpaste, etc, will result in secondary maturation, and the tooth enamel will gradually become more caries resistant.

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Dissolution of enamel

•The carious process is initiated by bacterial fermentation of carbohydrates, leading to the formation of a variety of organic acids and a fall in pH. •Initially, H + will be taken up by buffers in plaque and saliva, but, when the pH continues to fall (H + increases), the fluid medium will be depleted of OH- and PO3

4-, which react with H+ to form H2O and HPO2

4.

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 1. Intact block showing enamel surface and sub-surface

2. Beginning of  demineralization creates pores in the enamel resulting surface roughness and loss of shine. 

3. As demineralization progresses,  the pores increase and with remineralization the pores decrease.  

4. As the  pores enlarge bacteria may invade the subsurface.  It is somewhere during these stages of the demineralization process that the white spot lesion will lose its potential for remineralization.

5. In the final stage, the carious process has progressed to the point where sufficient amount of enamel matrix has been lost and the inward collapse of the remaining surface layer.     

Graphic representation of a block of enamel showing the surface and sub-surface enamel morphological changes in various stages of demineralization leading to white spot formation and finally to cavitation.

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•On total depletion, the pH can fall below the critical value of 5.5. where the aqueous phase becomes undersaturated with respect to hydroxyapatite. •Therefore, whenever surface enamel is covered by a microbial deposit, the on going metabolic processes within this biomass result in pH fluctuations, and occasional steep drops in pH, which may result in dissolution of the mineralized surface.

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•Dissolution of enamel can result in the development of either a carious lesion or erosion. •Caries is defined as the result of chemical dissolution of the dental hard tissues that is caused by bacterial degradation products, ie, acids produced by bacterial metabolism of low-molecular weight.

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•The erosive lesion is defined as dissolution of tooth substance, that is caused by any other acid-containing agent.

Massive Erosion from soft drink overuse 1 year later

Acid Erosion from reflux 

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•Mixed lesions may well exist, particularly when the dentin has been exposed by erosion, causing hypersensitivity, which may lead to inadequate plaque control and caries. This condition occurs frequently on exposed root surfaces.

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The appearance of the two lesions differs: •the carious lesion is characterized by a subsurface demineralized lesion body covered by a rather well-mineralized surface layer.

•In erosion, the surface has been etched away layer by layer. No subsurface demineralization can be seen in the erosive

lesion.

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•In principle, dental enamel can be dissolved under two different chemical conditions. •When the surrounding aqueous phase is unsaturated with respect to hydroxyapatite (HA) and supersaturated with respect to fluorapatite, HA dissolves and FA is formed. •The resulting lesion is a carious lesion in which the dissolving HA originates from subsurface enamel and FA is formed in the surface enamel layers.

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•The higher the supersaturation with respect to FA, the more fluoride is taken up in the enamel surface, the better mineralized the surface enamel layer becomes, and the less demineralized is the subsurface body of the lesion.•On the other hand, if there is undersaturation with respect to both HA and FA, both apatites dissolve concurrently, and layer after layer is removed. •This will result in an erosive lesion. Fresh acidic fruit, fruit juices, and acidic carbonated soft drinks are all unsaturated with respect to both apatites and are able to cause erosive demineralization of the teeth.

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• Progression of caries, from ultrastructural changes to visible decay, should be regarded as the cumulative effect of a long-alternating series of dissolution at low pH and partial reprecipitation when pH rises.

Eventually, after months or years, depending on the cariogenic challenge of the plaque, a clinically detectable white-spot lesion appears in the enamel. 

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Arrest of caries 

•Fluoride has a strong affinity for apatite, because of its small ionic size and strongly electronegative character.

•Two kinds of fluoride-apatite interaction occur: – incorporation into the crystal lattice and– binding to crystal surfaces.

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•Both interactions have important consequences for the solubility and dissolution properties of apatite.

•The rate at which carious lesions progress is clearly heavily dependent on the rate at which the apatite crystals dissolve.

•It has been shown that the dissolution rate can be reduced by fluoride even without any reduction in solubility of the bulk mineral. This effect is the basis for topical fluoride treatments.

•The presence of dissolved fluoride at concentrations as O.5 mg/L in acidic solutions causes a reduction in the dissolution rate of initially fluoride-free apatite. Furthermore, pretreatment of apatite crystallites with fluoride solutions significantly reduces the susceptibility of the apatite to acid dissolution.

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•These two effects are both the results of uptake of fluoride by the surfaces of the

apatite crystals.

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•During a cariogenic challenge, both the concentration of fluoride at the crystal surfaces and the fluoride concentration in the liquid phase are important.

•To reduce the dissolution rate, fluoridation of the crystal surfaces, by whatever means, is neccesary but the surface fluoridation will be maintained only if the solution bathing the crystals contains enough fluoride; otherwise, all parts of the crystal surfaces will dissolve.

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•Formation of CaF2 is possible at fluoride concentrations higher than 100 ppm, and the amount increases with:

– increasing fluoride activity, – prolonged exposure, and – lower pH in the solution.

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•Thus, significantly greater amounts of CaF2 are precipitated after a 4-minute application of a 2% sodium fluoride (NaF) solution than after a 2-minute mouth rinse with a 0.2% solution, and .....

•CaF2 formation is considerably increased after use of an acidulated phosphate fluoride solution, because of the enhanced availability of calcium ions dissolved from the dental apatite.

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•Modest amounts of CaF2 may be formed from the use of NaF dentifrices.

•In contrast, extremely high amounts of CaF2 may be expected from slow release fluoride varnishes with high fluoride concentration.

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•The precipitation of fluoride in early carious lesions, with the subsequent release of fluoride, is therefore believed to be a key mechanism for the caries-reducing effect of concentrated topical fluoride agents such as acidulated phosphate fluoride gels and varnishes (1% to 2% F).

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Remineralization •Mineral deposition in enamel defects such as the various

lesion may result in replacement of partial placement of the lost mineral and is therefore called remineralization.•White-spot or carious lesion remineralization is a widely documented phenomenon.

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•According to the literature, the “white spot" lesions undergo several changes in the clinic or in the laboratory. It may thus be transformed into a “brown spot" lesion, a remineralized lesion, an arrested lesion, and occasionally it even dissapears completely as a “caries reversal”.•Glossy appearance, surface increased hardness, missing porosity - are the features of. arrested, or remineralized lesions

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Three months later, there is a noticeable decrease in areas of demineralization and brown areas.

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ActivityAfter studying this lecture ...Write about ...What can I do as a dental student to help to prevent caries in my faculty, neighborhood, school...

D Caroline Mohamed 79

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Thank you

D Caroline Mohamed 80