Dental Caries - minia.edu.eg1)16-3 Semest… · caries yet might affect the progress of the carious...
Transcript of Dental Caries - minia.edu.eg1)16-3 Semest… · caries yet might affect the progress of the carious...
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Dental Caries
Dr: Maii Ibrahim Sholqamy
Lecturer of Oral Pathology Department
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1. Definition2. Contributing factors3. Roles of saliva 4. Classifications5. Theories6. Histopathology of
Dental caries
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Definition
a progressive irreversible bacterial damage of hard tooth structure
exposed to the oral environment.
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Characterized by
1) Demineralization of the inorganic portion
2) Destruction of the organic substances of the tooth
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InorganicMaterial
Organic Material
Tooth Structure
(Acid Formation)Demineralization
Dissolution
Caries Formation
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•Loss of tooth structure:
1.Attrition 2.Abrasion3.Erosion4.Dental caries
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Sequence of Dental Caries
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Contributing factors
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1)Position
2)Morphology
3)Structure and composition
4)Fluoride Content
5)Hereditary Factors
Factors affection Susceptibility of tooth to caries
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1) Position▪ Upper teeth ( Ant, Premolar), Lower teeth (Molars)
▪ Posterior teeth > Anterior teeth
▪Occlusal surface (molar), Proximal surface (Ant &
Premolars)
▪ Mal-posed, Rotated, Crowded teeth and tooth with
Orthodontic appliance (Stagnation areas)
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2) Morphology
▪Pits and fissures
▪The proximal contact point
▪Lingual and buccal convexities
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Pits and Fissure caries:V - type U - type I - type K - type
Deep pits and Fissures are more prone to caries :
1. Entrap of food and bacteria
2.Thin enamel accelerate exposing of dentine
3.Narrow and deep Poor self cleansing prosperities
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Proximal Contact area
The area below contact area is the most common site to dental caries as it provides good sheltered area for plaque formation.
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Proper site and contact is necessary to prevent dental caries
• Weak or slightly opened proximal contact causes food impaction.
• Too tight contact can damage the periodontal tissue.
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Too Narrow contact, Bucco-lingual or Occluso-gingivally
1.Food impaction vertically or horizontallyon col area.
2.Wide buccal and lingual embrasures inwhich normal hygiene measures aredifficult to be accessed resulting to foodretention and plaque accumulation inembrasure area
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Contact placed too gingivallyIt will Depth of occlusal embrasures Impingement of
Interdental col
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Loose (Open) contact area Leading to food impaction:
1.Accumulation of dental plaque 2.Periodontal diseases 3.Caries Problem
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Sites below Lingual and Buccal convexities
Convexity
Provide an inaccessible area
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3) Structure and Composition
Rate of Initiation and Progression of Caries.
Surface enamel more mineralized than subsurface
enamel
Enamel hypoplasia and enamel hypocalcification
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• It also accumulates more fluoride, zinc, lead ions than subsurfaceenamel. Therefore in initial carious lesions, the subsurface enamelshows marked demineralization even though the outer enamel isrelatively intact.
• The newly erupted teeth are generally caries susceptible until post-eruptive maturation is complete.
• Hypoplasia and hypocalcification do not affect the initiation ofcaries yet might affect the progress of the carious lesion.
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4) Fluoride Content
The fluoride content in tooth its resistance to dental caries.
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1. Reduction of apatite solubility :
Fluoride replaces the hydroxyl group in the hydroxyapatite forming
fluoroapatite which is less soluble in acids than hydroxyapatite and
thus more resistant to caries. ( Resistance to solubility)
These F ions will form:
1- Strong ionic bond with the ca ions
2- Hydrogen bond with the neighboring oH groups
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2. Enhancement of remineralization process of the carious lesion:
The presence of fluoride in the oral environment facilitates the
remineralization (repair) of the carious lesion by formation of
calcium-fluoro-phosphate salts
These salts render the remineralized site more resistant to future
acidogenic attacks than was the original enamel.
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3. Antibacterial activity.
• The effect of Fluoride is mainly on acidogenic bacteria.
• It inhibits bacterial enzymes (enolase) and thus stops bacterial
activities
This will lead to:
1- Decreased acid production.
2- Decreased glucose uptake by the organisms.
3- Decreased metabolic activity of the organisms
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5) Hereditary Factors
• It has minor effect
• Some families have low incidence caries
• Inheritance of favorable tooth shape and structure
• Difficult to exclude the role of dietary habits
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1- Susceptible TOOTH Surface
Position
Morphology
Structure and composition
Fluoride content
Hereditary
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1) Importance of Carbohydrates.
2) Factors affection cariogenicity of Carbohydrates
I. Type of CHO
II. Total amount of CHO
III. Frequency of CHO intake
IV. Consistency and texture of CHO
V. Refinement of CHO
3) Vipeholm experiment
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I. Type of CHO
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DisaccharidesSucrose (Arch criminal of caries)
1. The most consumed CHO
2. Low molecular weight, can diffuse rapidly into dental plaque.
3. It is readily metabolized by many bacteria involved in dentalbiofilm formation
4. Importance of Sucrose depends on the high energy of itsglucose-fructose
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Sucrose
Glucose Fructose
Dextran + Lactic acid
Levan + Lactic acid
Energy
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1. It has a lower pK constant
2. It causes a greater fall in pH thanequimolar solutions of acetic orpropionic acids that may also bedetected in plaque.
Lactic acid
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Extracellular Polysaccharides
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Extra cellular polysaccharides play a role in:
1. Formation of dental plaque
2. Increases adhesion of dental plaque on tooth surface andit is water insoluble so it is accumulated for a long time inthe plaque near tooth surface causing prolonged acidproduction when utilized by bacteria.
3. Extra cellular polysaccharides cause increased porosity ofdental plaque, leading to deep penetration of dietarysugars and greater acid production adjacent to the toothsurface.
4. Act as store for CHO
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Polysaccharides
•Are of no importance in the etiology of caries
1. They need the action of salivary amylase beforeoral bacteria can act on them.
2. They are of larger molecular weight and hence cannot diffuse readily and rabidly into dental plaque.
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II- Total amount of CHO
The total amount of CHO intake showed some little effect on caries.
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III. Frequency of CHO intake
• It refers to the number of times per day that sugary food eaten
• Frequent intake of CHO between meals will cause an increased caries incidence.
• That is because:
↑ period of availability of CHO
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IV. Consistency and texture of CHO
• Sucrose-containing fluids are quickly cleared from the mouthand less cariogenic
• Caries is not induced in susceptible animals if sucrose is fedonly by stomach-tube; its effect is entirely local
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• Sticky CHO are more cariogenic because:1) Slowly washed by saliva.2) They remain attached to tooth surface for longer time3) Remains accessible to the oral micro-organisms, with
more acid production
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V. Refinement of CHO
It is the treatment of CHO in order to make them :i. Remove fibrous material, vitamins and
mineralsii. Whiteriii.Improve flavor
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Refinement of CHO caries incidence:
•Remove fibrous material cleansing effect
• Concentrate the fermentable fraction of CHO
• adhesiveness of CHO
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Factors affection cariogenicity of CHO:
1. Type of CHO2. Total amount of CHO3. Frequency of CHO intake4. Consistency and texture of CHO5. Refinement of CHO
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3. Vipeholm experiment
1. Total CHO intake
2. Frequency of CHO intake
3. Texture and consistency
of CHO
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The final conclusions were that:
1) Frequency of administration ofCHO and consistency of CHOshowed a greater effect on cariesactivity.
2) Total CHO intake showed little
effect on caries activity.
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3- BACTERIA
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1)Miller Experiment
2)Orland Experiments
3)Types of bacteria involved in caries
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Tooth+
Carbohydrates incubation CARIES+ 37 °
Saliva
Tooth +
Carbohydrates Boiling NO CARIES+ 37 °
Saliva
1- Miller Experiment
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2- Orland Experiments
To confirm presence of BACTERIA for occurrence of caries
First Experiment 1954:He used Germ Free rats obtained by caesarian operationunder strict aseptic conditions.
Second Experiment 1955: He used Gnotobiote ratGnotobiot rat: are animals in which a single known strain ofmicro- organism was introduced.
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First Experiment
Germ free rat group + Sterile HIGHLY cariogenic diet
NO CARIES
Control rat group + Sterile HIGHLY cariogenic diet
CARIES
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Second Experiment
Streptococcus Mutans
Lactobacilli casei
Actinomycosis Israeli
Clostridia
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3- Types of Bacteria involved in caries
I. Acidogenic Bacteria
A- Streptococcus1. St. mutans2. St. sanguis3. St. salivarius4. St. mitis
B- Lactobacilli 1-L. acidophilous2-L. casei
II. Proteolytic Bacteria
A- Actinomycosis 1. Act. Viscose2. Act. Israeli3. Act bovis
B- ClostridiaC- Pseudomonas
III. Chromogenic Bacteria:
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1) Acidogenic2) Aciduric3) Have attachment mechanisms for firm adhesion to tooth
surface.4) Production of Extracellular polysaccharides for
formation of plaque matrix.5) Production of Intracellular polysaccharides for using in
CHO deficiency.
Cariogenic Bacteria
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A- Role of Streptococci
St. Mutans• A facultatively anaerobic, gram-positive coccus
• Commonly found in the human oral cavity
•
• Powerful Acidogenic
• Powerful Aciduric
• Have specific receptors
• Produce Extracellular polysaccharide and
Intracellular Polysaccharides
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Streptococci Mutans
Produce Smooth and Pits/fissure caries
• Sucrose St. mutans Glucose + Fructose + Energy
• Glucose St. mutans Dextran + Lactic acidglucosyltransferase
• Fructose Levan + Lactic acidfructosyltransferase
St. mutans
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Extracellular Polysaccharides
LevanDextran
Fructose PolymerGlucose polymer
Water SolubleWater Insoluble
Less adhesiveHighly adhesive
Act as a store of Carbohydrates
Important in plaque formation and porosity
of it
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• St. Mutans can synthesize andstore an intracellular glycogen –like polysaccharide known asamylopectin
• The Intracellular Polysaccharidesare used by the micro-organism attimes of dietary CHO deficiency.
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Role of Lactobacilli
• Powerful acidogenic bacteria
• Powerful Aciduric bacteria
• They are mild proteolytic
• Their number increase in saliva when caries activity is increased.
• Lactobacilli Pits and fissure caries
Smooth caries why?
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Conclusions
•St. mutans Smooth caries
Pits and fissure caries
Root caries
•Lactobacilli Pits and fissure caries
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4- Dental Plaque
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Definition:
• Soft, non-mineralized, tenaciously adherent bacterial deposit on teeth and dental prostheses
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• Plaque becomes visible, particularly on the labial surfaces of theincisors, when toothbrushing is stopped for 12–24 hours.
• It appears as a translucent film with a matt surface that dulls theotherwise smooth and shiny enamel.
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• Resists cleansing by physiological oral forces like:
1. Salivary washing,
2. Friction of food during mastication and
3. Tongue movements
But is removable by tooth brushing.
• However, neither toothbrushing nor fibrous foods will removeplaque from inaccessible surfaces or pits (stagnation areas). Thistenacious adherence is mediated by the matrix polysaccharides
• It is considered as a contributing factor for at least initiation ofcaries, but presence of dental plaque doesn‘t necessarily meancaries will occur
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Types:
1) Supragingival Dental Caries
2) Supgingival Periodontal Diseases
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Dental Plaque Biofilm
1) Internal Surface Salivary component (Pellicle)
2) External Surface Contact with oral cavityContain Bacteria
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• Plaque is a biofilm of bacteria embedded in an extracellularpolysaccharide matrix
• Biofilms are multi-cellular communities formed by bacteria, andthey consist of bacteria encased within a non-crystallineextracellular matrix (ECM) of proteins, polysaccharides, and smallmolecules.
• Biofilm formation provides increased protection of bacteria fromantibiotics and host defenses.
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• A biofilm may be resistant to antimicrobials or to immunological
defenses to which the individual bacterial species are normally
sensitive.
• The biofilm traps and concentrates bacterial products, favoring
survival and interactions between species.
Bacterial plaque must therefore be regarded as a living ecosystem
and not as a mere collection of bacteria
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Composition of dental plaque
Micro-organism
Inorganic saltsCa, ph, k, Mg, Na, Fe, Cu, zn
and FL
Water 80%Solid 20%
OrganicProteins
CarbohydratesLipids
Extracellular matrix
Desquamated epithelium
Food debris
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Mechanism of Formation
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Stage I: Deposition of the acquired pellicle
• Definition : organic, acellular, structurless, bacterial-free film of salivary origin.
• Salivary glycoprotein (Protein + Carbohydrate) which is Selective Adsorbed onhydroxyapatite of the tooth surface (for about 3µm).
• Rate of formation of the pellicle varies in individuals due to differences in salivaryflow and composition
• This selective adsorption depends on the positive or negative charge found on theapatite molecule. In other words a positively charged apatite molecule will attracta negatively charged glycoprotein and a negatively charged apatite molecule willattract a positively charged glycoprotein.
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• The job of the pellicle is to:1. Prevent acids from attacking the teeth and2. Releasing the minerals therein.3. Just like a lubricating film, it protects teeth when chewing
from abrasion caused by food or the other teeth
•Acquired pellicle acts as a substrate for adherence,nutrition, growth and colonization of plaque micro-organism.
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Stage II: Colonization of the acquired pellicle
• Acquired pellicle becomes visible, when tooth brushing stops for 12-24hours and by proliferated of heterogenous bacterial flora occurs.
• Adhesion of bacteria to the tooth surfaces is an essential requirement.
• Attachment depends on complex mechanism and again on bacterialproduction of extracellular polysaccharides such as glucans (dextran).
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• Pioneer bacteria which colonize the pellicle coated tooth surfaceare St. sanguis and actinomycosis viscosis. They are potentprotease.
1. These are enzymes that can digest the protein coat on themicroorganisms themselves and on some sites on the enamel surface.
2. By this way the charges on the microbial cell wall and on the apatitecrystal become exposed, and attachment of the microorganisms to theenamel surface is achieved.
• Some of these pioneer microorganisms release extracellularenzymes capable of liberating the carbohydrate group from thepellicle glycoproteins.
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I-Growth phase
• The initial bacterial colonies grow in size and coalesce witheach other forming a monolayer of microorganisms coveringthe enamel pellicle.
• Further bacterial growth is in a vertical direction formingcolumns of bacteria radiating perpendicular to the toothsurface.
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II- Intermediate community
This begins with the ingress and proliferation of secondary invaders (St. mutans) this will lead to:
1. Fermentation of sucrose with the production of acids. It is powerfulaciduric (+ ve interaction) while, St. sanguis will disappear as they areless aciduric (- ve interaction).
2. Synthesis of ECP. As a result other organisms will be attached to theplaque
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Stage III: Maturation of the dental plaque
• Proliferation of heterogeneous bacterial flora leading to increase inthe thickness of the dental plaque, oxygen consumption in deeperlayers will cause anaerobic filamentous microorganisms to colonizethe plaque
• The filamentous microorganisms grow in long interlacing threads inwhich smaller bacilli and cocci become entrapped.
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Functions:
1- It provides adhesiveness, bulk and nutrition for bacterialmetabolism to produce acid for a long time.
2- Acting as diffusion limiting membrane thus retaining lactic acid inhigh concentration at particular site for a long time.
3- The same diffusion limiting effect may also slow down the entryof buffers from saliva, thus delaying their neutralizing action.
4- It is necessary for smooth surface caries and root caries
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Acid production in the Plaque(Stephan Curve)
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The rapidity with in pH :
1.Rapid diffusion of sugar intoplaque.
2.Activity of the large amount ofenzymes produced by the greatnumber of bacteria in theplaque
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• Further drop of the pH below the critical level may be due to:
1. Breakdown of the reservepolysaccharides in the plaque.
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The slow reversion to the resting pH:
1. Continued metabolism of residualsugars absorbed by the plaque
2. Delayed diffusion of acids outwardinto saliva
3. Delayed diffusion of salivarybuffers into plaque
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The rate of plaque formation varies in different persons according to:
1. Position and anatomy of the tooth.
2. Presence of appliances.
3. Structure of the tooth.
4. Friction from diet
5. Oral hygiene procedures.
6. Composition of the diet.
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Biochemical reactions in the Plaque
1)Acid Production
2)Formation of extracellular polysaccharides
3)Formation of intracellular polysaccharides
4)Demineralization phase
5)Remineralization phase
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Saliva & Dental Caries
• Saliva is a complex secretion :1. Rate of flow,
2. Composition
3. Properties
• Saliva has a critical role in caries
prevention.
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Composition of Saliva
• Volume: 600 – 1000 ml/day• Electrolytes: calcium, bicarbonate, sodium, potassium,
chloride and magnesium• Secretory proteins: Amylase, proline rich proteins , mucin
lysozyme and lactoferrin• Immunoglobins: IgA, Ig G and Ig M• Small organic: Glucose, amino acids, urea, uric acid and lipid
molecules.• Other components: Epidermal growth factor
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1. Formation of acquired enamel pellicle:Salivary glycoproteins acquired enamel pellicle
2. Washing effect of saliva:The flow of saliva act as cleansing effect for bacteria and food
3. Buffering effect of saliva:Salivary buffers (mainly carbonic acid/bicarbonate system) neutralize the PH fall (acidity).
The buffering power of saliva is related to the rate of secretion
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4. Remineralization of carious lesion:
Calcium, phosphate and fluoride in saliva diffuse into the plaque reducing the solubility of enamel and promoting the remineralization of the caries lesion.
5. Salivary antibodies:
Secretory immunoglobulin A (s IgA)
1. Killing or inhibition of bacterial growth
2. Prevention of adherence of bacteria to tooth surfaces
6. Antibacterial substance:
lysozymes, peroxides and lactoferrin have a direct anti-bacterial action on plaque micro-organisms.
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Dental Caries
Dr: Maii Ibrahim Sholqamy
Lecturer of Oral Pathology Department
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1. Definition2. Contributing factors3. Roles of saliva 4. Classifications5. Theories6. Histopathology of
Dental caries
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Definition
a progressive irreversible bacterial damage of hard tooth structure
exposed to the oral environment.
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Characterized by
1) Demineralization of the inorganic portion
2) Destruction of the organic substances of the tooth
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InorganicMaterial
Organic Material
Tooth Structure
(Acid Formation)Demineralization
Dissolution
Caries Formation
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•Loss of tooth structure:
1.Attrition 2.Abrasion3.Erosion4.Dental caries
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Sequence of Dental Caries
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Contributing factors
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1)Position
2)Morphology
3)Structure and composition
4)Fluoride Content
5)Hereditary Factors
Factors affection Susceptibility of tooth to caries
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1) Position▪ Upper teeth ( Ant, Premolar), Lower teeth (Molars)
▪ Posterior teeth > Anterior teeth
▪Occlusal surface (molar), Proximal surface (Ant &
Premolars)
▪ Mal-posed, Rotated, Crowded teeth and tooth with
Orthodontic appliance (Stagnation areas)
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2) Morphology
▪Pits and fissures
▪The proximal contact point
▪Lingual and buccal convexities
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Pits and Fissure caries:V - type U - type I - type K - type
Deep pits and Fissures are more prone to caries :
1. Entrap of food and bacteria
2.Thin enamel accelerate exposing of dentine
3.Narrow and deep Poor self cleansing prosperities
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Proximal Contact area
The area below contact area is the most common site to dental caries as it provides good sheltered area for plaque formation.
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Proper site and contact is necessary to prevent dental caries
• Weak or slightly opened proximal contact causes food impaction.
• Too tight contact can damage the periodontal tissue.
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Too Narrow contact, Bucco-lingual or Occluso-gingivally
1.Food impaction vertically or horizontallyon col area.
2.Wide buccal and lingual embrasures inwhich normal hygiene measures aredifficult to be accessed resulting to foodretention and plaque accumulation inembrasure area
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Contact placed too gingivallyIt will Depth of occlusal embrasures Impingement of
Interdental col
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Loose (Open) contact area Leading to food impaction:
1.Accumulation of dental plaque 2.Periodontal diseases 3.Caries Problem
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Sites below Lingual and Buccal convexities
Convexity
Provide an inaccessible area
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3) Structure and Composition
Rate of Initiation and Progression of Caries.
Surface enamel more mineralized than subsurface
enamel
Enamel hypoplasia and enamel hypocalcification
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• It also accumulates more fluoride, zinc, lead ions than subsurfaceenamel. Therefore in initial carious lesions, the subsurface enamelshows marked demineralization even though the outer enamel isrelatively intact.
• The newly erupted teeth are generally caries susceptible until post-eruptive maturation is complete.
• Hypoplasia and hypocalcification do not affect the initiation ofcaries yet might affect the progress of the carious lesion.
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4) Fluoride Content
The fluoride content in tooth its resistance to dental caries.
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1. Reduction of apatite solubility :
Fluoride replaces the hydroxyl group in the hydroxyapatite forming
fluoroapatite which is less soluble in acids than hydroxyapatite and
thus more resistant to caries. ( Resistance to solubility)
These F ions will form:
1- Strong ionic bond with the ca ions
2- Hydrogen bond with the neighboring oH groups
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2. Enhancement of remineralization process of the carious lesion:
The presence of fluoride in the oral environment facilitates the
remineralization (repair) of the carious lesion by formation of
calcium-fluoro-phosphate salts
These salts render the remineralized site more resistant to future
acidogenic attacks than was the original enamel.
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3. Antibacterial activity.
• The effect of Fluoride is mainly on acidogenic bacteria.
• It inhibits bacterial enzymes (enolase) and thus stops bacterial
activities
This will lead to:
1- Decreased acid production.
2- Decreased glucose uptake by the organisms.
3- Decreased metabolic activity of the organisms
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5) Hereditary Factors
• It has minor effect
• Some families have low incidence caries
• Inheritance of favorable tooth shape and structure
• Difficult to exclude the role of dietary habits
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1- Susceptible TOOTH Surface
Position
Morphology
Structure and composition
Fluoride content
Hereditary
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1) Importance of Carbohydrates.
2) Factors affection cariogenicity of Carbohydrates
I. Type of CHO
II. Total amount of CHO
III. Frequency of CHO intake
IV. Consistency and texture of CHO
V. Refinement of CHO
3) Vipeholm experiment
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I. Type of CHO
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DisaccharidesSucrose (Arch criminal of caries)
1. The most consumed CHO
2. Low molecular weight, can diffuse rapidly into dental plaque.
3. It is readily metabolized by many bacteria involved in dentalbiofilm formation
4. Importance of Sucrose depends on the high energy of itsglucose-fructose
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Sucrose
Glucose Fructose
Dextran + Lactic acid
Levan + Lactic acid
Energy
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1. It has a lower pK constant
2. It causes a greater fall in pH thanequimolar solutions of acetic orpropionic acids that may also bedetected in plaque.
Lactic acid
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Extracellular Polysaccharides
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Extra cellular polysaccharides play a role in:
1. Formation of dental plaque
2. Increases adhesion of dental plaque on tooth surface andit is water insoluble so it is accumulated for a long time inthe plaque near tooth surface causing prolonged acidproduction when utilized by bacteria.
3. Extra cellular polysaccharides cause increased porosity ofdental plaque, leading to deep penetration of dietarysugars and greater acid production adjacent to the toothsurface.
4. Act as store for CHO
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Polysaccharides
•Are of no importance in the etiology of caries
1. They need the action of salivary amylase beforeoral bacteria can act on them.
2. They are of larger molecular weight and hence cannot diffuse readily and rabidly into dental plaque.
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II- Total amount of CHO
The total amount of CHO intake showed some little effect on caries.
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III. Frequency of CHO intake
• It refers to the number of times per day that sugary food eaten
• Frequent intake of CHO between meals will cause an increased caries incidence.
• That is because:
↑ period of availability of CHO
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IV. Consistency and texture of CHO
• Sucrose-containing fluids are quickly cleared from the mouthand less cariogenic
• Caries is not induced in susceptible animals if sucrose is fedonly by stomach-tube; its effect is entirely local
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• Sticky CHO are more cariogenic because:1) Slowly washed by saliva.2) They remain attached to tooth surface for longer time3) Remains accessible to the oral micro-organisms, with
more acid production
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V. Refinement of CHO
It is the treatment of CHO in order to make them :i. Remove fibrous material, vitamins and
mineralsii. Whiteriii.Improve flavor
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Refinement of CHO caries incidence:
•Remove fibrous material cleansing effect
• Concentrate the fermentable fraction of CHO
• adhesiveness of CHO
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Factors affection cariogenicity of CHO:
1. Type of CHO2. Total amount of CHO3. Frequency of CHO intake4. Consistency and texture of CHO5. Refinement of CHO
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3. Vipeholm experiment
1. Total CHO intake
2. Frequency of CHO intake
3. Texture and consistency
of CHO
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The final conclusions were that:
1) Frequency of administration ofCHO and consistency of CHOshowed a greater effect on cariesactivity.
2) Total CHO intake showed little
effect on caries activity.
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3- BACTERIA
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1)Miller Experiment
2)Orland Experiments
3)Types of bacteria involved in caries
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Tooth+
Carbohydrates incubation CARIES+ 37 °
Saliva
Tooth +
Carbohydrates Boiling NO CARIES+ 37 °
Saliva
1- Miller Experiment
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2- Orland Experiments
To confirm presence of BACTERIA for occurrence of caries
First Experiment 1954:He used Germ Free rats obtained by caesarian operationunder strict aseptic conditions.
Second Experiment 1955: He used Gnotobiote ratGnotobiot rat: are animals in which a single known strain ofmicro- organism was introduced.
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First Experiment
Germ free rat group + Sterile HIGHLY cariogenic diet
NO CARIES
Control rat group + Sterile HIGHLY cariogenic diet
CARIES
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Second Experiment
Streptococcus Mutans
Lactobacilli casei
Actinomycosis Israeli
Clostridia
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3- Types of Bacteria involved in caries
I. Acidogenic Bacteria
A- Streptococcus1. St. mutans2. St. sanguis3. St. salivarius4. St. mitis
B- Lactobacilli 1-L. acidophilous2-L. casei
II. Proteolytic Bacteria
A- Actinomycosis 1. Act. Viscose2. Act. Israeli3. Act bovis
B- ClostridiaC- Pseudomonas
III. Chromogenic Bacteria:
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1) Acidogenic2) Aciduric3) Have attachment mechanisms for firm adhesion to tooth
surface.4) Production of Extracellular polysaccharides for
formation of plaque matrix.5) Production of Intracellular polysaccharides for using in
CHO deficiency.
Cariogenic Bacteria
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A- Role of Streptococci
St. Mutans• A facultatively anaerobic, gram-positive coccus
• Commonly found in the human oral cavity
•
• Powerful Acidogenic
• Powerful Aciduric
• Have specific receptors
• Produce Extracellular polysaccharide and
Intracellular Polysaccharides
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Streptococci Mutans
Produce Smooth and Pits/fissure caries
• Sucrose St. mutans Glucose + Fructose + Energy
• Glucose St. mutans Dextran + Lactic acidglucosyltransferase
• Fructose Levan + Lactic acidfructosyltransferase
St. mutans
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Extracellular Polysaccharides
LevanDextran
Fructose PolymerGlucose polymer
Water SolubleWater Insoluble
Less adhesiveHighly adhesive
Act as a store of Carbohydrates
Important in plaque formation and porosity
of it
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• St. Mutans can synthesize andstore an intracellular glycogen –like polysaccharide known asamylopectin
• The Intracellular Polysaccharidesare used by the micro-organism attimes of dietary CHO deficiency.
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Role of Lactobacilli
• Powerful acidogenic bacteria
• Powerful Aciduric bacteria
• They are mild proteolytic
• Their number increase in saliva when caries activity is increased.
• Lactobacilli Pits and fissure caries
Smooth caries why?
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Conclusions
•St. mutans Smooth caries
Pits and fissure caries
Root caries
•Lactobacilli Pits and fissure caries
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4- Dental Plaque
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Definition:
• Soft, non-mineralized, tenaciously adherent bacterial deposit on teeth and dental prostheses
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• Plaque becomes visible, particularly on the labial surfaces of theincisors, when toothbrushing is stopped for 12–24 hours.
• It appears as a translucent film with a matt surface that dulls theotherwise smooth and shiny enamel.
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• Resists cleansing by physiological oral forces like:
1. Salivary washing,
2. Friction of food during mastication and
3. Tongue movements
But is removable by tooth brushing.
• However, neither toothbrushing nor fibrous foods will removeplaque from inaccessible surfaces or pits (stagnation areas). Thistenacious adherence is mediated by the matrix polysaccharides
• It is considered as a contributing factor for at least initiation ofcaries, but presence of dental plaque doesn‘t necessarily meancaries will occur
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Types:
1) Supragingival Dental Caries
2) Supgingival Periodontal Diseases
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Dental Plaque Biofilm
1) Internal Surface Salivary component (Pellicle)
2) External Surface Contact with oral cavityContain Bacteria
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• Plaque is a biofilm of bacteria embedded in an extracellularpolysaccharide matrix
• Biofilms are multi-cellular communities formed by bacteria, andthey consist of bacteria encased within a non-crystallineextracellular matrix (ECM) of proteins, polysaccharides, and smallmolecules.
• Biofilm formation provides increased protection of bacteria fromantibiotics and host defenses.
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• A biofilm may be resistant to antimicrobials or to immunological
defenses to which the individual bacterial species are normally
sensitive.
• The biofilm traps and concentrates bacterial products, favoring
survival and interactions between species.
Bacterial plaque must therefore be regarded as a living ecosystem
and not as a mere collection of bacteria
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Composition of dental plaque
Micro-organism
Inorganic saltsCa, ph, k, Mg, Na, Fe, Cu, zn
and FL
Water 80%Solid 20%
OrganicProteins
CarbohydratesLipids
Extracellular matrix
Desquamated epithelium
Food debris
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Mechanism of Formation
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Stage I: Deposition of the acquired pellicle
• Definition : organic, acellular, structurless, bacterial-free film of salivary origin.
• Salivary glycoprotein (Protein + Carbohydrate) which is Selective Adsorbed onhydroxyapatite of the tooth surface (for about 3µm).
• Rate of formation of the pellicle varies in individuals due to differences in salivaryflow and composition
• This selective adsorption depends on the positive or negative charge found on theapatite molecule. In other words a positively charged apatite molecule will attracta negatively charged glycoprotein and a negatively charged apatite molecule willattract a positively charged glycoprotein.
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• The job of the pellicle is to:1. Prevent acids from attacking the teeth and2. Releasing the minerals therein.3. Just like a lubricating film, it protects teeth when chewing
from abrasion caused by food or the other teeth
•Acquired pellicle acts as a substrate for adherence,nutrition, growth and colonization of plaque micro-organism.
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Stage II: Colonization of the acquired pellicle
• Acquired pellicle becomes visible, when tooth brushing stops for 12-24hours and by proliferated of heterogenous bacterial flora occurs.
• Adhesion of bacteria to the tooth surfaces is an essential requirement.
• Attachment depends on complex mechanism and again on bacterialproduction of extracellular polysaccharides such as glucans (dextran).
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• Pioneer bacteria which colonize the pellicle coated tooth surfaceare St. sanguis and actinomycosis viscosis. They are potentprotease.
1. These are enzymes that can digest the protein coat on themicroorganisms themselves and on some sites on the enamel surface.
2. By this way the charges on the microbial cell wall and on the apatitecrystal become exposed, and attachment of the microorganisms to theenamel surface is achieved.
• Some of these pioneer microorganisms release extracellularenzymes capable of liberating the carbohydrate group from thepellicle glycoproteins.
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I-Growth phase
• The initial bacterial colonies grow in size and coalesce witheach other forming a monolayer of microorganisms coveringthe enamel pellicle.
• Further bacterial growth is in a vertical direction formingcolumns of bacteria radiating perpendicular to the toothsurface.
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II- Intermediate community
This begins with the ingress and proliferation of secondary invaders (St. mutans) this will lead to:
1. Fermentation of sucrose with the production of acids. It is powerfulaciduric (+ ve interaction) while, St. sanguis will disappear as they areless aciduric (- ve interaction).
2. Synthesis of ECP. As a result other organisms will be attached to theplaque
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Stage III: Maturation of the dental plaque
• Proliferation of heterogeneous bacterial flora leading to increase inthe thickness of the dental plaque, oxygen consumption in deeperlayers will cause anaerobic filamentous microorganisms to colonizethe plaque
• The filamentous microorganisms grow in long interlacing threads inwhich smaller bacilli and cocci become entrapped.
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Functions:
1- It provides adhesiveness, bulk and nutrition for bacterialmetabolism to produce acid for a long time.
2- Acting as diffusion limiting membrane thus retaining lactic acid inhigh concentration at particular site for a long time.
3- The same diffusion limiting effect may also slow down the entryof buffers from saliva, thus delaying their neutralizing action.
4- It is necessary for smooth surface caries and root caries
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Acid production in the Plaque(Stephan Curve)
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The rapidity with in pH :
1.Rapid diffusion of sugar intoplaque.
2.Activity of the large amount ofenzymes produced by the greatnumber of bacteria in theplaque
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• Further drop of the pH below the critical level may be due to:
1. Breakdown of the reservepolysaccharides in the plaque.
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The slow reversion to the resting pH:
1. Continued metabolism of residualsugars absorbed by the plaque
2. Delayed diffusion of acids outwardinto saliva
3. Delayed diffusion of salivarybuffers into plaque
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The rate of plaque formation varies in different persons according to:
1. Position and anatomy of the tooth.
2. Presence of appliances.
3. Structure of the tooth.
4. Friction from diet
5. Oral hygiene procedures.
6. Composition of the diet.
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Biochemical reactions in the Plaque
1)Acid Production
2)Formation of extracellular polysaccharides
3)Formation of intracellular polysaccharides
4)Demineralization phase
5)Remineralization phase
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Saliva & Dental Caries
• Saliva is a complex secretion :1. Rate of flow,
2. Composition
3. Properties
• Saliva has a critical role in caries
prevention.
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Composition of Saliva
• Volume: 600 – 1000 ml/day• Electrolytes: calcium, bicarbonate, sodium, potassium,
chloride and magnesium• Secretory proteins: Amylase, proline rich proteins , mucin
lysozyme and lactoferrin• Immunoglobins: IgA, Ig G and Ig M• Small organic: Glucose, amino acids, urea, uric acid and lipid
molecules.• Other components: Epidermal growth factor
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1. Formation of acquired enamel pellicle:Salivary glycoproteins acquired enamel pellicle
2. Washing effect of saliva:The flow of saliva act as cleansing effect for bacteria and food
3. Buffering effect of saliva:Salivary buffers (mainly carbonic acid/bicarbonate system) neutralize the PH fall (acidity).
The buffering power of saliva is related to the rate of secretion
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4. Remineralization of carious lesion:
Calcium, phosphate and fluoride in saliva diffuse into the plaque reducing the solubility of enamel and promoting the remineralization of the caries lesion.
5. Salivary antibodies:
Secretory immunoglobulin A (s IgA)
1. Killing or inhibition of bacterial growth
2. Prevention of adherence of bacteria to tooth surfaces
6. Antibacterial substance:
lysozymes, peroxides and lactoferrin have a direct anti-bacterial action on plaque micro-organisms.