introduction caries flouride

وقاية \ اسنان خامس

د. خولة م(1-3)
8-12-2016
وقاية \ اسنان خامس
د. خولة م(1-3)
8-12-2016

preventive dentistry

the science of the care required to prevent disease of the teeth and supporting structures. There are three levels of preventive dentistry: the use of a topical fluoride gel to prevent caries is an example of primary prevention, a dental restoration is anexample of secondary prevention, and a fixed bridge is an example of tertiary prevention.
1. that branch of the healing arts concerned with the teeth and associated structures of the oral cavity, including prevention, diagnosis, and treatment of disease and restoration of defective or missing teeth.
the work done by dentists, e.g., the creation of restoration, crowns, and bridges, and surgical procedures performed in and about the oral cavity.
the practice of the dental profession collectively

Primary prevention.

It is concerned with offering information on potential health threat to healthy members of the population. Such advice will enable individuals to avoid unnecessary risk factors, the primary preventive services is that prevents the initiation of disease(pre pathogenesis stage).

These services are designed as ones which provide health promotion and specific protection.


Health promotion activities such as providing instructions about proper plaque removal or daily flossing are designed to promote general optimum health in this case periodontal health also dietary advice to control dental caries.

Specific protective activities include those that are designed to protect against disease agents by establishing barrier against agents in the environment. The ingestion of optimum fluoridated water and application of occlusal sealants provide specific protection against dental caries.

Secondary Prevention

The services in this level are directed toward the initial stages of the disease .These services intervene or prevent the progression and recurrence of the disease, they are designed as activities that are aimed at early diagnosis and promote treatment of disease in order to prevent sequel , ex, promote treatment of small carious lesion will result in the prevention of extended loss of tooth structer.

Tertiary Prevention.

Its services are directed towards the end results of the disease , they are referred to as replacement services that prevent loss of function , these activities are divided in to ;
1.Disability limitation
2. Rehabilitation.
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Dental caries
Is a multi factorial disease in which there is an interaction of four principle factors for the formation of the disease
The host (teeth and saliva)
Micro flora
Substrate(diet)
Time


So caries requires a susceptible host ,a cariogenic oral flora and suitable diet , all theses must be present for sufficient length of time , intervention or removal of any necessary factors may prevent the disease.

Managing caries in enamel

Dental caries is process which may take place on any tooth surface in the oral cavity where a microbial bio film (dental plaque) is allowed to develop over a period of time.
Formation of the biofilm is a natural physiological process .It is important to remember that the bio film is not a haphazard collection of micro-organisms, but a community with a collective physiology , which can solve the specific physic-chemical problems posed by the environment at the site .The bacteria in the bioflim are always metabolically active , causing minute fluctuations in PH. These may cause a net loss of mineral from the tooth .
Alternatively , there may be a net gain of mineral when the PH is increasing When the PH is dropping . This is called demineralization
.The cumulative result of these de- and remineralization processes may be a net loss of mineral and a carious lesion that can be seen .Alternatively , the changes may be so slight that a carious lesion never becomes apparent.

The formation of the biofilm and its metabolic activity cannot be prevented , but disease progression can be controlled so that a clinically visible . enamel lesion never forms . management depends on appreciating that the de. and remineralization processes can be modified . for instance , if the biofilm is partially or totally removed . mineral loss may be stopped or even reversed toward mineral gain . keyes (1954) was the first to explain the interplay between local cariogenic bacteria in plaque , fermentable carbohydrates constitutional factors (related to species and strains ) and tooth structure .Dental caries was shown to be an infectious process of teeth with the interplay of three principal factors ;the host ,microflora and diet .Even though knowledge of the biological determinants and the interactions among the different factors has increased, this model is still valid today .

Factors which influence the magnitude of the pH fluctuations

Are also very important and many of these can be influenced
The composition and thickness of the microbial deposits
The diet
Fluoride ion concentration .
The salivary secretion.
These biological factors can in turn be influenced by various sociological parameters such as a person s behavior, attitudes, their knowledge and beliefs .

The carious process and the carious lesion

Carious lesions can form on any tooth surface exposed to the mouth ;thus they can form on enamel ,cementum , or dentine .principles of management of the process are the same ,irrespective of the tooth tissue involved .
The term caries can be used to refer to both caries process and the the caries lesion that forms as a result of that process.


The concept of activity
1 . The caries process may or may not be progressive .
2. Lesions may be active .
3. Lesions may be arrested by diet , oral hygiene and use of fluorides.

Caries risk assessment

Factors relevant to assessment of caries risk
High risk Low risk
Social l history
Socially deprived middle class
High caries in Siblings low caries in siblings
Low knowledge of disease dentally aware
Irregular dental attendance regular dental attendance
Snacking very much no regular snacking
2. Medical history
Medically compromised No problem medically
Disabled No physical problem
Xerostomia Normal flow of saliva
Medicinal syrups for long period of time. No long term medication
3. Dietary habit
Frequent intake of sugar Infrequent intake of sugar
4.Fluorides
Non fluoridated area Fluoridated area
No fluoride supplements. Fluoridated supplements
No fluoridated toothpaste Fluoridated toothpaste
5.plaque control
Infrequent , ineffective Frequent , effective cleaning
Poor manual dexterity Good manual dexterity
6.Saliva
Low flow rate Normal flow rate
Low buffer capacity High buffering capacity
Increased counts of S. mutan. Low counts of Str.mutan
Increased Lacto. Counts. Low counts of lactobacillus
7. Clinical evidence
-New lesions evident No new lesions
-Premature extraction of No extractions of primary
primary
-Anterior caries or No or very few restorations
restorations
-Repeated restorations Restorations inserted years
with no recurrent caries
No fissure sealants Fissure sealants present
Orthodontic appliances , fixed No orthodontic,fixed or removable prosthesis prosthesis
Site predilection for the cries process
Any surface where the microbial biofilm remains undisturbed
Partially erupted teeth
Depth of the fissure system
A proximally , below the contact point.
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Mode of Action of Fluoride or Mechanism of Caries Control of Fluoride

Fluorides acts in several different ways to reduce dental caries action and this multiplicity of effects is the key to caries prevention action.

Enamel crystal structure or change of the tooth structure during tooth formation.

The principle mineral substance in enamel (also dentine and bone) is the hydroxyl apatite (HA), however, the F ions has a strong affinity for mineralized tissue, and HA can be readily converted into fluoro apatite (FA) when F has replaced hydroxyl group and this takes place during periods of tooth formation and calcification.
The relative proportion of FA to HA in enamel is varies, with a higher proportion of FA in outer enamel in enamel exposed to F solution or covered with plaque for a long period.
Changes in tooth structures include:
The HA crystals tended to possess voids and such voids were likely to increase crystal reactivity, so they dissolve more readily and easily. The F ion eliminate the voids and stabilize the crystal structure. So enamel with FA resists demineralizatios and dissolution of enamel.
Apatite crystals tend to be surrounded by a hydration layer which may include other ions such as magnesium, carbonate and fluoride. But magnesium and carbonate unlike F, are associated with poor crystallinity and a further favorable reaction of F would appear to be the ability to replace magnesium and carbonate in the apatite crystals so making the crystal more stable.
Incorporation of F also tend to increase the size of the crystal, this would result in a decrease in crystal surface area per unit volume and therefor reduce the rate of enamel dissociation. So the increase in F concentration in enamel is either while the apatite crystals of the tooth are forming(systemic F administration) or after the enamel is formed and the tooth has erupted into the oral cavity (topical administration).

Bacteriostatic effect of fluoride

F has inhibition effect on enzymes especially glycolytic enzyme like (enolase) and inhibit glycolysis, the process by which sugar is metabolized by bacteria to produce acid.
There is also some evidence that F inhibit the production of extra poly saccharide (dextran) by cariogenic bacteria, necessary process for plaque adherence to smooth surfaces.
A further possible mechanism, there is evidence that F may has specific bactericidal action on cariogenic bacteria in the plaque especially in higher concentration and a low PH.
F concentration is necessary for reduction of acid production. Even a low concentration of F (1-2 ppm) are able to produce detectable reduction in acid production, 10 ppm produce moderately large reduction in acid production and 100 ppm completely inhibit bacterial growth.
The amount of available F is several times greater in F rich than in low F area in dental plaque, so the bacteria of dental plaque formed in fluoridated area when exposed to levels of F that can inhibit further acid formation, while those of plaque formed in non-fluoridated areas are not. Thus the PH values of plaque formed in low F is much less, so loss of enamel minerals occurs when plaque is low in F and this loss is reduced when plaque F level is high.

Remineralization

It may be defined as a deposit of minerals or inorganic substances in an area from which such substances were previously removed.
In early stages of carious lesion (chalky) the lesion is not simply a process of demineralization, but it characterized by alternating periods of destruction and repair.
During the carious process of demineralization of enamel, apatite is reduced to simpler compounds or ions, but during a subsequent remineralization phase, the apatite will again be formed.
Apatite is the most stable and least soluble of biologic calcium phosphate compounds and its formation during mineralization phase is therefore desirable. One of the most important actions of F is its ability to increase the formation of apatite during remineralization.
A researcher suggested that during remineralzation the outer layer of the apatite crystals may take up F so that it acquires the property of fluoroapatite.
Possibly due to F ability to enhance remineralization of carious enamel, F becomes incorporated into the new crystal structure and increased in amount over many years.


Epidemiological evidence of remineralization in vivo
Many studies noted that white spot lesion of caries may become arrested or retarded under favorable oral conditions.
In a study, the examination of 184 buccal surfaces of maxillary first molars in same children at age 8 and again at age 15 years, of 72 surfaces with white spots at 8 years, 37 appeared sound at age of 15.

Evidence of remineralization from experimental caries in man

When block of enamel covered with Teflon gauze to facilitate bacterial colonization were mounted in movable partial denture in the human mouth, the enamel block showed surface softening as detected by micro hardness test. When the gauze was removed to expose the enamel to the saliva in vivo, an increase of hardness occurred in the block. This increased in hardness was thought due to remineralization.
Recently, an experiment using the same method of producing experimental caries, a fluoride solution was used to encourage remineralization, subsequently the healed lesion was again covered with gauze to create a cariogenic environment, the enamel which had remineralized was now found to be more resistant to dental caries than adjacent areas of sound enamel. It thus seems possible that a remineralized white spot lesion may be more resistant to carious attack than sound enamel. This cycle could occur many times, each time resulting in increased concentration of fluoride in the new enamel and a reduced susceptibility to future caries attack.
Other experiment, the subject used sucrose mouth rinse for 23 days to induce caries.After this time, oral hygiene procedures were recommended and subjects used daily mouth rinses with 0.2% NaF solution for 1 month. Caries scores showed regression or healing of the experimental lesion during the F mouth rinses regime.

Remineralization evidence in vitro

In this technique, the researcher used micro hardness testing to measure the quantitative changes in enamel surface. In these experiments, first the sound human teeth were tested for hardness and then tested after softening with an acetate buffer solution and retested again after exposure to remineralization solution and saliva which contain calcium, phosphate and fluoride ions. In this experiments it was assumed that the rehardening of the enamel surface was indicative for remineralization.

Alteration in morphology of teeth

Teeth in fluoride areas had shallow fissures and well developed well rounded cusps and some times where 2% smaller.

Delayed eruption of teeth in fluoridated areas

Little support for this hypothesis

How do topical fluoride works

Several mechanisms have been postulated and it is entirely probable that a combination of these works together to arrest a preventive effect.
Formation of fluoro apatite which cause the enamel to become more resistant to dissociation by bacterial acids (most common hypothesis)
Fluoride enriched enamel which begins to dissolve in bacterial acids liberates a quantity of fluoride sufficient to retard the demineralization process and to promote remineralization.
The frequent application of topical fluoride can reduce the relative quantity of cariogenic microorganisms in plaque especially streptococcus mutans. This is due to direct action of topical fluoride agent on bacteria or due to indirect route involving fluoride released from enamel or plaque as a result of bacterial acid accumulation.
The less important suggestion is that fluoride treatment of the teeth will lower the enamel free surface energy to make plaque accumulation more difficult or could even desorb bacteria from hydroxyl apatite.