cariology

Designed by Al-Wasifi, Y.A.

CARIOLOGYThe Science of Dental Caries

By:

The Staff Members of Operative Dentistry Division

Department of Restorative Dental ScienceCollege of DentistryTaibah UniversityKSA

CARIOLOGY OPERATIVE DENTISTRY, COLLEGE OF DENTISTRY, TAIBAH UNIVERSITY, KSA Designed by Al-Wasifi, Y.A.


Intended Learning Outcomes (ILOs)

BY THE END OF THIS PRESENTATION, YOU SHOULD BE ABLE TO:1. Define dental caries.2. Recognize participants of dental caries etiology.3. List different theories explaining the incidence of dental

caries.4. Clarify the rationale of dental caries ecology.5. Clarify the rationale of adhesion to enamel and dentin.6. List the different factors contributing for dental caries.7. Classify different type of dental caries.8. Recognize the role of fluoride in dental caries prevention.9. List different methods of fluoride application.10.Recognize the rationale of dental plaque control.11.List different methods of dental plaque control.


CARIOLOGY OPERATIVE DENTISTRY, COLLEGE OF DENTISTRY, TAIBAH UNIVERSITY, KSA

DEFINITIONS &

INTRODUCTION


DEFINITIONS & INTRODUCTION

Dental caries is a disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth.


DEFINITIONS & INTRODUCTION

Dental caries is considered a disease of modern civilization.

Extensive studies had been made of the incidence of dental caries, in existing primitive races and it was noted that the incidence was invariably less than that in civilized man.

These studies indicate that modern civilization and increased dental caries are constant in their association and that primitive isolated tribes are relatively caries – resistant.


DEFINITION & INTRODUCTION

Apart from age and the advance of civilization, many other factors influence the prevalence and incidence of dental caries in populations.

These include:1. Dietary habits.2. Race.3. Geographical locations.4. Sex.5. Familial patterns.6. Influence of treatment.



Dental Caries is:

1. Site-specific: caries occurs in areas of food stagnation where plaque can accumulate and remain undisturbed.

2. Multifactorial: that involves the shift of the balance between protective factors (that aid in remineralization) and destructive factors (that aid in demineralization) to favor demineralization of the tooth structure over time.



Dental Caries is:

3. Dynamic: a state of demineralization & demineralization, but not necessarily continuous.

4. Disease process: Involves microorganisms.

5. Can be arrested at any point in time.



ETIOLOGY OF DENTAL CARIES



“The complete divorcement of dental practice from studies of the pathology of dental caries, that existed in the past, is an anomaly in science that should not continue. It has the apparent tendency plainly to make dentists mechanics only”

G.V. Black, 1908



ACID

InorganicOrganic


AGENDAa) ETIOLOGICAL THEORIES OF

DENTAL CARIES.b) ECOLOGY OF DENTAL CARIES.c) FACTORS CONTRIBUTING FOR

DENTAL CARIES.d) DIFFUSION PHENOMENON.





ETIOLOGICAL THEORIES OF DENTAL

CARIES


ETIOLOGICAL THEORIES

A complete explanation of how the dental caries destroys the teeth has not yet been found.Historically, it was thought to be due to:1. Worm theory (7000 BC – 1700’s).2. Vital theory (1700’s): Inflammation within the

tooth that leads to necrosis, gangrene and finally amputation of the tooth.



Recently many theories were developed to explain how caries destroys the tooth structure:

a) ACIDOGENIC THEORY.b) PROTEOLYTIC THEORY.c) PROTEOLYTIC CHELATION

THEORY


ETIOLOGIC THEORIES A) ACIDOGENIC THEORY

Assigned and proposed by Miller and also known as Miller’s theory.

• Cariogenic bacteria produce acid that decalcifies the inorganic tooth structure.

• The caries process continues by breakdown of the organic cementing substance by numerous micro organisms.





THEORY


ETIOLOGIC THEORIES B) PROTEOLYTIC THEORY

Assigned and proposed by Gottlieb, et al.

• Proteolytic micro organisms of the oral cavity have the ability to invade the organic part of the tooth structure liberating a proteolytic enzymes (collagenase and keratinase enzymes) that destroy the collagen matrix of the tooth structure.

• The formed acid could then demineralize the inorganic part.





THEORY


ETIOLOGIC THEORIES C) PROTEOLYTIC CHELATION THEORY

Assigned and proposed by Schatz.

• Liberated acids with the help of chelating agents could demineralize the inorganic part.

• Bacterial proteolytic enzymes destruct the organic matrix.




ECOLOGY OF DENTAL CARIES



A better understanding of dental caries can be obtained by viewing dental disease as a consequence of an ecological system.

Ecology: Is the science that studies interaction between organisms and their environment.

Ecosystem: It is a circumscribed area occupied by biological community, e.g. Oral cavity.

Habitat: Constitutes an area where food and shelter for supporting different species of microorganisms (organism location or address) e.g. Dental fissure.

So, the ecosystem is formed of different habitats.



Ecological niche: Organism profession, i.e. what it does to survive.

• For each habitat, a limited number of niches are available to the oral flora.

• St. Mutans is the microorganism of dental caries, so if the niches are not available by any mean, St. Mutans could be prevented from being established leading to decrease in dental caries production.




FACTORS CONTRIBUTING FOR

DENTAL CARIES


FACTORS CONTRIBUTING FOR DENTAL CARIES

• Some plaque bacteria are capable of fermenting a suitable dietary carbohydrate substrate to produce acid, causing the plaque pH to fall below 5 within 1 – 3 minutes.

• Repeated falls in pH may result in the demineralization of a susceptible site on a tooth surface, thus initiating the carious process.



The factors contributing to this process are:

I. Dental plaque. II. Dietary carbohydrates. III. Susceptibility of the tooth surface. IV. Time.


FACTORS CONTRIBUTING I. DENTAL PLAQUE

Definition:• Dental plaque is an adherent deposit of bacteria

and their products, which forms on all tooth surfaces.



Formation:• When a clean enamel surface is exposed to the

oral environment it becomes covered with an amorphous organic film called the pellicle.

• This consists mainly of a glycoprotein precipitated from saliva, which is very tenacious, and can attract and help anchor specific types of bacteria to the tooth structure.

• A large proportion of these is a streptococcus but only about 2% of these are mutans streptococci.



Formation (Cont.):• This is interesting because, these microorganisms

are particularly associated with initiation of the carious process.

• Within few days the plaque becomes thicker and a mixture of different types of microorganisms comprise the bacterial community.

• Consequently, the flora of the plaque changes from its initial predominantly coccal form to a mixed flora consisting of cocci, rods and filaments.



Formation (Cont.):• There are local variation in the micro-flora at

different sites on the tooth surface and these differences may explain why some sites experience a high caries activity while neighboring sites in the same mouth remain relatively free from clinically detectable caries.



Role of bacteria:• Mutans streptococci and lactobacilli are

cariogenic because they are able to produce acid rapidly from fermentable carbohydrates (acidogenic).

• They thrive under acid conditions (aciduric) and are able to adhere to the tooth surface because of their ability to synthesize sticky extracellular polysaccharides from dietary sugars.



Role of bacteria (Cont.):• These polysaccharides, which are mainly

polymers of glucose, give the matrix of dental plaque its gelatinous consistency.

• Consequently, they help: 1. Bacteria to stick to each other and to the

tooth. 2. Thickening the layer of plaque. 3. Preventing saliva from neutralizing plaque

acid.



Plaque Hypothesis:

There are two hypothesizes:

1. Non-specific plaque hypothesis considered any plaque responsible for carious process and daily mechanical plaque removal is important.

2. Specific plaque hypothesis depend on dental plaque not always cariogenic and there are certain plaque that are colonized by specific microorganisms responsible for dental caries.


FACTORS CONTRIBUTING II. DIETARY CARBOHYDRATES

• Carbohydrates provide the plaque bacteria with the substrate for acid production and the synthesis of extracellular polysaccharides.

• However, carbohydrates are not all equally cariogenic.

• While complex carbohydrates such as starch are relatively harmless because they are not completely digested in the mouth, the low molecular weight carbohydrates (sugars) diffuse readily into plaque and are metabolized quickly by the bacteria.



• Thus many sugar containing foods and drinks cause a rapid drop in the plaque pH to a level which can cause demineralization of dental enamel.

• The plaque remains acid for some time, taking 30 – 60 minutes to return to its normal pH in the region of “7”.

• The gradual return of pH to baseline values is a result of acid diffusion out of the plaque and buffers in the plaque and salivary film overlaying it, exerting a neutralizing effect.



• Repeated and frequent consumption of sugars will keep plaque pH depressed and cause demineralization of the teeth.

• The synthesis of extracellular polysaccharides from sucrose is more rapid than from glucose, fructose and lactose.

• Consequently, sucrose is the most cariogenic sugar, although the other sugars are also harmful.

• Since sucrose is also the sugar eaten most commonly, it is a very important cause of dental caries.


FACTORS CONTRIBUTING III. SUSCEPTIBILITY OF TOOTH SURFACE

• Bacterial plaque is an essential precursor of caries, and for this reason, sites on the tooth surface which favor plaque retention and stagnation are particularly prone to decay.

• These sites are: 1. Enamel pits and fissures.2. Approximal enamel smooth surfaces just

cervical to the contact point.3. The enamel of the cervical margin of the tooth

just coronal to the gingival margin.



4. In patients where periodontal disease has resulted in gingival recession, the area of plaque stagnation is on the exposed root surface.

5. The margins of restorations, particularly those that are deficient or overhanging.

6. Tooth surfaces adjacent to dentures and bridges, which increase the areas, where stagnation can occur.



ENVIRONMENT OF THE TOOTH

a) Saliva b) Fluoride



A) SALIVAUnder normal conditions, the tooth is continually bathed in saliva.Since the susceptibility of the tooth to caries depends to a large extent on its environment, saliva has a considerable part to play.It is capable of remineralizing the early carious lesion because it is supersaturated with calcium and phosphate ions.This remineralizing capacity of saliva is enhanced when the fluoride ions are present.



A) SALIVA (CONT.)When salivary flow is diminished or absent there is increased food retention.

Since salivary buffering capacity has been lost, a low pH environment is encouraged and persists longer.

This is turn encourages aciduric bacteria, which relish the acid conditions, and continues to metabolize carbohydrate in the low pH environment.



B) FLUORIDE

The presence of optimum concentrations of fluoride in the environment and in the dental tissues exerts an anti-caries effect in several ways.

The most important mechanism is probably its ability to retard the rate of progression of the lesion.


FACTORS CONTRIBUTING IV. TIME

• The carious process consists of alternating periods of destruction and repair, and the saliva has the ability to delay progression of lesions.

• Thus, when saliva is present, caries does not destroy the tooth in days or weeks but rather in months or years, or not at all.




DIFFUSION PHENOMENON



Featherstone, et al, in 1980, formulated the diffusion phenomenon to explain the process of dental caries.

Diffusion phenomenon is based on the acidogenic theory but with slight modification.



The mechanism of dental caries according to Featherstone diffusion phenomenon is:

1. Organic acids as lactic acid are formed by carbohydrate metabolism in plaque.

2. The acids will diffuse through the enamel due to concentration gradient passing through the acquired pellicle.

3. The diffusion will be firstly through the inter-prismatic area, and then the water filled areas of the organic matrix.



4. Acids will dissociate giving hydrogen and (-)ve radicals which attack the apatite lattice of enamel forming calcium and phosphorous complex.

5. According to concentration gradient calcium and phosphorous will diffuse outwards in unionized form giving rise to demineralization with subsequent cavity formation


Enamel



Enamel

DIFFUSION PHENOMENONAcid

Acid

Minerals

Minerals

Acid

Acid

PO4---

Ca+

+

F-F-

F-

F-PO4---

PO4---Ca+

+

Ca+

+

Ca+

+


Enamel

DIFFUSION PHENOMENONAcid

Acid

Minerals

PO4---

Ca++

F-F-

F-

F-PO4---

PO4---

PO4---

Ca++

Ca++

Ca++

Minerals

Minerals

Minerals

Acid

Acid

Minerals

Minerals



CLASSIFICATION OF

DENTAL CARIES


CLASSIFICATION OF DENTAL CARIES

Dental caries could be classified according to:

a) The anatomical site.b) The attack.c) The invasion.d) The extent.e) The onset.f) The visibility and degree of destruction.g) The severity of carious challenge.


CLASSIFICATION A) THE ANATOMICAL SITE

Stagnation area that accumulate carbohydrates.

1. Pits &

Fissure surface

Which may start on enamel or on the exposed root cementum or dentin.

2. Smooth surface


CLASSIFICATION A) THE ANATOMICAL SITE

Capillary Attraction Theory


CLASSIFICATION B) THE ATTACK

Which is the first attack of caries in previously sound healthy tooth surface.

1. Primary Caries

Which is the secondary caries attack to a tooth surface previously restored developed at the margins of the restoration.

2. Recurrent Caries


CLASSIFICATION B) THE ATTACK

Recurrent Caries

Caries Invitation Caries extension


CLASSIFICATION C) THE INVASION

When the spread of caries along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the DEJ and termed backward caries.

1. Backward Caries

Forward caries is whenever the caries cone in enamel is larger or at least the same size as that of dentin.

2. Forward Caries


CLASSIFICATION D) THE EXTENT

The first evidence of caries activity in the enamel, that is not extended to the dentino-enamel junction, and the enamel surface is fairly hard and still intact.The lesion can be remineralized if immediate corrective measures alter the oral environment, including plaque removal and control. This lesion, then, may be stated as reversible.

1. Incipient

Caries

In cavitated caries the lesion has advanced into dentin, the enamel surface is broken (not intact), and remineralization is not possible. Treatment by cavity preparation and restoration is indicated.May be stated as irreversible.

2. Cavitated Caries


CLASSIFICATION E) THE ONSET

Painful, lightly discolored and soft in consistency.

Histologically, the acid penetration proceeds bacterial invasion, i.e. the last layer is affected by acids but not infected by microorganisms.

1. Acute Caries

Painless, due to increased chance for formation of reparative dentin, dark or brownish discoloration and hard in consistency.

Bacterial invasion proceeds or coincides with acid penetration; i.e. the last layer is both affected by acid decalcification and infected by microorganisms.

2. Chronic Caries



Special Clinical Forms of Acute Caries

a) Rampant Caries

It is the name given to a sudden rapid destruction of many teeth, frequently involving surfaces of teeth that are usually caries – free.

It may be seen in permanent teeth of teenagers and is usually due to taking frequent cariogenic snacks and sweet drinks between meals.




a) Rampant Caries (Cont.)

It is also seen in mouths where there is a sudden marked reduction in salivary flow (xerostomia). Radiation in the region of salivary gland, used in the treatment of malignant tumors, is the most common cause of an acute xerostomia.



a) Rampant Caries (Cont.)




Special Clinical Forms of Acute Cariesb) Nursing Caries

It is a particular form of rampant caries in the primary dentition of infants and young children.

It is found in an infant or toddler who falls asleep sucking a bottle (called a nursing bottle) which has filled with sweetened fluids (including milk).

The frequency of sugar intake combined with a low salivary flow at night are important in the development of this form of rampant caries.



Special Clinical Forms of Acute Cariesb) Nursing Caries (Cont.)

The clinical pattern is characteristic, with the four maxillary deciduous incisors most severely affected.



Special Clinical Forms of Chronic Caries

a) Arrested Caries

This term describes a carious lesion, which does not progress.

It is seen when the oral environment has changed from conditions predisposing to caries, to conditions that tend to arrest the lesion.



Special Clinical Forms of Chronic Caries

a) Arrested Caries (Cont.)


CLASSIFICATION F) THE VISIBILITY & DEGREE OF DESTRUCTION

Showing a slight destruction in enamel due to short period of time.

1) Shallow Cavity:

Showing destruction of enamel up to DEJ.

2) Moderate Cavity:

Showing destruction of enamel and dentin approaching the pulp tissues due to long period of time.

3) Deep Cavity:


CLASSIFICATION G) THE SEVERITY OF CARIOUS CHALLENGE

In which only the most vulnerable teeth and surfaces are attacked, such as cervical margin of the teeth or pits and fissures of molar teeth.

In which carious lesions involving also the approximal surfaces of teeth.

In which the anterior teeth which normally remain caries – free, also becomes carious.

1) Mild Challenge:

2) Moderate Challenge:

3) Severe Challenge:



PREVENTION OF

DENTAL CARIES


Prevention or control of dental caries could be achieved by one or both of the following:

a) FLUORIDE SUPPLEMENTATION.b) CONTROL OF DENTAL PLAQUE.

PREVENTION OF DENTAL CARIES



A) FLUORIDE SUPPLEMENTATION



AGENDAI. CRYSTALLINE STRUCTURE OF

ENAMEL.II. DEPOSITION OF FLUORIDE IN

ENAMEL.III. CARIOSTATIC MECHANISM OF

FLUORIDE.IV. FLUOROSIS.V. FLUORIDE APPLICATION.VI.FLUORIDE TOXICITY.



A) FLUORIDE SUPPLEMENTATION I. CRYSTALLINE STRUCTURE OF ENAMEL

• Enamel mineral is crystalline and has a lattice structure characteristic of hydroxyapatite, the smallest repeating unit of which can be expressed by the formula Ca10 (PO4) (OH)2.

• However, it is not a pure hydroxyapatite since it also has a non-apatite phase (amorphous calcium phosphate or carbonate).



Cross sectionof rods in mature

human enamel

Hexagon-shaped enamel crystallites



• Additional ions or molecules are adsorbed on to the large surface area of the apatite crystals.

• This can happen in several different ways:1. The crystal lattice has the capacity to substitute

other ionic species of appropriate size and charge.

Thus within the lattice, calcium can be exchanged for radium, strontium, lead, and hydrogen ions while phosphate can be exchanged for carbonate, and hydroxyl for fluoride.



2. Sodium, magnesium, and carbonate can be substituted or adsorbed at the crystal surface.

3. There may be defects present in the internal lattice.

4. It is also possible for part of the lattice to be lost without the whole crystal disintegrating.

Similarly, remineralization can occur.


A) FLUORIDE SUPPLEMENTATION II. DEPOSITION OF FLUORIDE IN ENAMEL

There is a great deal of scope to affect the fluoride concentration of enamel since it can be deposited in three stages of enamel development:

1) Low concentrations, reflecting the low levels of fluoride in tissue fluids, are incorporated in the apatite crystals during their formation.

2) After calcification is complete, but before eruption, more fluoride is taken up by the surface enamel which is in contact with the tissue fluids.

3) Finally, after eruption and throughout life, the enamel continues to take up fluoride from its external environment.


A) FLUORIDE SUPPLEMENTATION II. DEPOSITION OF FLUORIDE IN ENAMEL

• Any increase in porosity facilitates the diffusion and uptake of fluoride by enamel.

• The fluoride content of intact surface enamel is much higher than the interior enamel but tends to be extremely variable.

• It varies between primary and permanent teeth, between different individuals living in the same area, between different teeth in the same individual, and even between different surfaces of the same tooth.

• In carious enamel, white-spot or brown-spot 1esions, fluoride levels are raised whereas in areas worn by attrition the levels are low.


A) FLUORIDE SUPPLEMENTATION III. CARIOSTATIC MECHANISM OF FLUORIDE

1. The presence of fluoride ions greatly enhances the precipitation of fluoroapatite from calcium and phosphate ions present in saliva making enamel more acid resistant.

2. Fluoride inhibits enolase enzyme essential for completion of the process of glycolysis.

3. Fluoride ion inhibits glycosyl transferase, that prevents the polymerization of glucose to form extracellular polysaccharides with subsequent reduction of bacterial adhesion to tooth structure.


A) FLUORIDE SUPPLEMENTATION III. CARIOSTATIC MECHANISM OF FLUORIDE

4. Fluoride ions used in topical fluoride application are directly toxic to some microorganisms including S. mutans, suppression of growth of S. mutans following single topical fluoride application may last several weeks.

5. Fluorides alter the surface energy of enamel rendering it less susceptible for adhesion of bacteria.

6. Fluoride accelerates the clearance of glucose in saliva.

7. Fluoride minimizes the transportation of sucrose to inside the bacterial cell.


A) FLUORIDE SUPPLEMENTATION IV. FLUOROSIS

Signs:• The first sign of excessive intake of fluoride

during the period of tooth formation is the eruption of teeth with fluorosed or mottled enamel.

• Its appearance varies from fine white lines in the enamel to chalky, opaque enamel, which turns brown, or black after eruption.

• The enamel may even break apart soon after tooth eruption.



Mild Fluorosis Moderate Fluorosis Severe Fluorosis



Mechanism:• The exact mechanism is not fully understood, but

fluoride is thought to affect ameloblast function during both the secretory and the maturation phases, leading to defective mineralization.

• Fluorosis can be caused by a single high fluoride dose, lower but multiple doses, and by low-level continuous exposure.

• Consequently, it can be produced by ingestion of fluoride from the drinking water and toothpaste as well as by use of dietary fluoride supplements.



Mechanism (Cont.):• Although permanent teeth go on developing from

birth to adolescence, it is the anterior teeth that are of most concern from an aesthetic viewpoint.

• Thus, the most critical time is from birth to 8 years but the risk is greatest during the first two years of life.


A) FLUORIDE SUPPLEMENTATION V. FLUORIDE APPLICATION

Fluoride Application

I. Systemic II. Topical

1. Drinking water2. Fluoride tablets3. Fluoridated salt4. Fluoridated Milk5. Pre-natal fluoride

a) Frequent – UseLow Concentration

b) Periodic – UseHigh Concentration

1. Tooth paste2. Mouth rinses

1. Sodium fluoride varnish2. APF gel3. Stannous fluoride gel4. Prophylaxis paste


A) FLUORIDE SUPPLEMENTATION VI. FLUORIDE TOXICITY

• Anyone recommending the use of fluoride-containing dental preparations should be aware of the fluoride content and the potential hazards.

• The exact mechanism by which fluoride produces its toxic effect is not known.

Symptoms of sub-lethal poisoning:1. Salivation, nausea and vomiting. 2. The symptoms usually appear within an hour of

ingestion.



Management:• A small quantity of fluoride (less than 5 mg/kg

body weight) is neutralized by drinking a large volume of milk.

• If more than 5 mg/kg have been ingested or if there is any doubt about the exact quantity consumed, the child should be taken to hospital and given gastric lavage.



Although no cases of acute toxicity due to ingestion of toothpaste have ever been reported, a 5-year-old could be severely poisoned by consuming about two-thirds of a 100-ml tube of 1500-ppm fluoride paste; a 1-year-old would need to consume only half this amount.

Fluoride toothpaste should therefore be kept out of the reach of young children.


Prevention or control of dental caries could be achieved by one or both of the following:

a) FLUORIDE SUPPLEMENTATION.b) CONTROL OF DENTAL PLAQUE.




B) CONTROL OF DENTAL PLAQUE



AGENDAI. REVIEWING PLAQUE

HYPOTHESIS.II. METHODS OF PLAQUE

CONTROL.



B) CONTROL OF DENTAL PLAQUE I. REVIEWING PLAQUE HYPOTHESIS

a) Non-specific plaque hypothesis:

• It suggests that all plaque is potentially cariogenic.

• This would imply that daily mechanical plaque removal is important in the management of the carious process.



b) Specific plaque hypothesis:• It proposes that plaque is not always cariogenic

and that only certain plaques, colonized by specific microorganisms, are responsible for dental decay.

• This would imply that targeting of specific organisms, such as mutans streptococci, might control the carious process.

• This approach is the rationale behind considering the use of topical antimicrobials such as chlorhexidine, in the management of dental caries.



c) Ecological plaque hypothesis:• It combines the two previous approaches. • The argument behind the ecological plaque

hypothesis can be summarized as follows:

1. Cariogenic bacteria are found naturally in dental plaque.

2. At neutral pH these organisms are a small proportion of the total plaque community.

3. With a conventional diet, the processes of de- and remineralization are in equilibrium and the carious process does not progress.

4. If the frequency of carbohydrate intake increases, plaque spends more time at an acid pH.



c) Ecological plaque hypothesis (Cont.):5. This low pH favors the proliferation of mutans

streptococci and lactobacilli and tips the balance towards demineralization.

6. Now greater numbers of mutans streptococci and lactobacilli in plaque produce acid at faster rates, enhancing demineralization.

• This hypothesis explains the lack of total specificity in the microbial etiology of dental caries.

• It explains the pattern of bacterial succession and shows why both the approach of total plaque removal and chemical targeting of specific microorganisms may have a role to play in the management of dental caries.


AGENDAI. REVIEWING PLAQUE

HYPOTHESIS.II. METHODS OF PLAQUE

CONTROL.



B) CONTROL OF DENTAL PLAQUE II. METHODS OF PLAQUE CONTROL

Methods of Plaque Control

a) Mechanical b) Chemical

1. Seeing Plaque.

2. Tooth Brushes.3. Inter-dental Cleaning.4. Dentifrices.

1. Chlorhexidine.

2. Enzymes.3. Surface active agents.4. Antibiotics.

5. Antibacterial agents.



• In order to learn how to remove plaque effectively it is helpful for the patient to see where it is present.

• Since plaque is translucent and has a color similar to teeth, it must be stained in order to be seen clearly.

• Liquids, tables, and capsules containing erythrosin or vegetable dyes are used to stain plaque and are called ‘disclosing agents’.

• The disclosing agent should be applied after tooth brushing so that areas where oral hygiene is inadequate can be seen easily.

a) Mechanical1. Seeing Plaque



• Tooth brushes vary widely in shape and size of the head, the material, texture, and arrangement of filaments as well as in the size and shape of the handles.

• However, at present nearly all tooth brushes available are multi-tufted with nylon filaments.

• It is particularly important that brushes are replaced regularly, at least every three months or sooner if the bristles become permanently bent.

• However, for the physically handicapped, where manual dexterity is limited, an electric tooth brush is very helpful.

a) Mechanical2. Tooth Brushes



• Approximal surfaces and areas where teeth are maligned cannot be reached with an ordinary tooth brush.

• Consequently, additional aids such as dental floss or tape, woodsticks, single-tufted brushes, or inter-dental brushes may be required for these areas.

• Choice will depend on the shape of the inter-dental area and the dexterity of the individual.

a) Mechanical3. Inter-Dental Cleaning



• In the past dentifrices were used in conjunctions with a tooth brush solely for cosmetic and social reasons.

• However, in the last 30 years fluorides, antibiotics, ammonium compounds, enzyme inhibiting dental caries, were added.

• Of all these agents only fluoride has stood up to clinical testing for safety and efficacy in caries prevention.

• It is also becoming increasingly common for manufacturers to add other therapeutic or preventive agents to reduce gingivitis and calculus formation.

• A few toothpaste also contain desensitizing agents.

a) Mechanical4. Dentifrices



Mechanism of action:• Chlorhexidine is an antiseptic belonging to the

chemical group of compounds called bisbiguanides, which are bactericidal and fungicidal.

• It has a broad spectrum of activity against gram-positive and gram-negative organisms as well as yeast.

• The chlorhexidine molecule is cationic, which means it is positively charged and because of its positive charge, it is attracted to bacterial cell walls, which are negatively charged.

• The bacterial cell wall is then irreversibly damaged with subsequent precipitation of its cytoplasmic components, resulting in cell death.

b) Chemical1. Chlorhexidine



Side - Effects:1) Staining:• The most conspicuous side effect is the

development of yellow/brown stain on the teeth and tongue and on the margins of anterior restorations.

• Staining around these restorations can be prevented if they are coated with Vaseline before rinsing.

• The stain is caused by the interaction of chlorhexidine with certain constituents of the diet.

• This limits the long-term use of chlorhexidine.




2) Taste:• Chlorhexidine has a bitter taste and there is a

general dulling of taste sensation for a few minutes to several hours after rinsing.

• The bitter taste has been masked quite successfully by flavoring agents.

3) Parotid gland swelling:• A few cases of unilateral or bilateral swelling of

the parotid glands have been reported. • However, they were all reversible when rinsing

was discontinued.




4) Desquamation of oral mucosa:• Few cases of painful desquamatous lesions have

been reported. 5) Long-term effects:• There is a slight change in the balance of oral

flora in favor of the organisms that are less sensitive to it, but this returns to normal after three months.




Indications:1. Individuals who have been assessed to be at high

risk to active caries. This assessment should be made on the basis of

history, clinical and radiographic examination, dietary history, salivary secretion rate, and buffer capacity.

2. Patients with greatly reduced salivary flow, who are consequently very much at risk to caries, benefit from the prophylactic use of chlorhexidine in conjunction with fluoride.




Indications:

3. May also be used prophylactically to prevent the transmission of cariogenic microorganisms from parents to children and from primary teeth to the permanent dentition.




• Hydrolytic, proteolytic, and glycolytic enzymes have been tested in attempts to break down the plaque matrix and so cause disruption and dispersal of the plaque.

• So far these attempts have proved ineffective or impractical due to: 1. The complex nature of the inter-microbial

matrix of dental plaque.2. The specificity and short duration of action of

some of these enzymes.

b) Chemical2. Enzymes



• In vitro studies show that fluoride may be capable of retarding the deposition of pellicle and plaque although there is little evidence in vive to support this.

• Attempts have been made to form moisture-repellent coatings on the smooth surfaces of tooth.

• Preliminary studies using the amine-substituted alcohols have been encouraging.

b) Chemical3. Surface Active Agents



• Antibiotics are important for the treatment of more serious infections so that the potential dangers associated with sensitization and the development of resistant strains of organisms as well as super-infection by fungal organisms prohibit their use for routine plaque.

b) Chemical4. Antibiotics



a) Fluoride:• The effect of fluoride on plaque bacteria and

bacterial metabolism has been discussed. • The daily home use of fluoride at such a high

concentration cannot be generally recommended because of safety considerations.

• Although lower concentrations of fluoride can affect bacterial metabolism the bactericidal effect of the concentrations used in dentifrices and mouthwashes remains to be confirmed.

b) Chemical5. Anti Bacterial Agents



b) Triclosan:• Triclosan has a broad spectrum of anti-microbial

activity against yeast and gram-positive and gram-negative bacteria.

• Although it has been shown to reduce plaque deposition and gingivitis to some extent, its value as a cariostatic agent is not yet proven adequately.




c) Metal ions:• Zinc, thin, and copper have shown some anti-

plaque activity. • Adverse reactions related to clinical use are an

unpleasant metal taste with a feeling of dryness and some staining.



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caries resistant

different factors

list different theories

disease of modern civilization