Dental Caries

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Dental Caries by Mind Map: Dental Caries

1. Definition

1.1. caries is a progressive, irreversible bacterial destruction of hard tooth structure present in the oral cavity

1.2. specific types of bacteria produce acids and cause demineralization of the inorganic portion of tooth followed by collapse of the organic

1.3. caries may progress through enamel, dentin and into the pulp and result in inflammaton of the pulp and later periapical tissue

2. Types of dental caries

2.1. 1. Pits and fissure caries

2.1.1. the most common

2.1.2. on occlusal surface and buccal surface of molars in teeth

2.1.3. most destructive form of caries, it goes quickly deep in the dentine

2.2. 2. Smooth surface caries

2.2.1. less common and occurs on interproximal areas of tooth that are not self cleansin

2.2.2. sometimes on carvical region of buccal and lingual surface of teeth

2.3. 3. Cemental (root) caries

2.3.1. in old population with gingival recession

2.3.2. this type provides difficulties to clinicians because it's located on region where there is little tooth structure

2.4. 4. Recurrent caries

2.4.1. arises around an existing restoration

2.4.2. due to alteration in integrity of restoration causing marginal leakage

2.5. 5. Acute rampant and chronic caries

2.5.1. denote rate of caries progress

2.5.2. young patients are susceptible to acute or rampant because they have teeth with large pulp chambers and wide and short dentinal tubules with no sclerosis

2.5.3. associated with diet rich in carbs

2.5.4. Chronic is common in old patients with teeth with small pulpal chamber with dense less tubular dentine called 2ry dentine

3. Factors Contribulting to Caries

3.1. 1- Susceptible tooth structure

3.2. 2- Saliva

3.3. 3- Fermentable carbohydrates

3.4. 4- Micro-organisms

3.5. 5- Dental Plaque

4. 1- Susceptible tooth structure

4.1. 1- Position of tooth

4.1.1. upper more prone than lower

4.1.2. molars and premolars more than anterior

4.1.3. creation of stagnation areas due to crowding of teeth or malposed teeth or presence of clasps  , orthodontic appliance increases susceptibility to caries

4.2. 2- Morphology of tooth

4.2.1. some create stagnation areas like pits and fissures, areas below proximal contact points, below lingual convexities

4.3. 3- structure

4.3.1. Dev Defects

4.3.1.1. developmental defects eg Enamel hypoplasia en enamel hypocalcification affect only rate of progression not inititiation

4.3.2. Age

4.3.2.1. caries progress rapidly in newly erupted teeth but later resistance of tooth increases due to post eruptive maturation which occurs due to hypermineralization and increase fluoride content

4.3.3. Fluoride

4.3.3.1. fluoride may be incorprated in development of teeth before eruption. after eruption fluoride content increase at surface due to post eruptive maturation thus increasing reistance

4.3.3.2. ingestion of fluoride content in conc more than 1.5 ppp 1mg fluoride/ liter at time of mineralization associated with enamel fluorosis ( mottling of enamel)  hypoplastic enamel due to toxic effect of fluoride on ameloblast

4.3.3.3. mottled enamel although hypoplastic is more resistant to caries

4.3.3.4. present in

4.3.3.4.1. drinking water

4.3.3.4.2. sea food

4.3.3.4.3. topical application

4.3.3.5. Cariostatic effect by

4.3.3.5.1. 1- it replaces hydroxyl group in HAP formin fluoroapetite which is less soluble in acids so it is more resistant to caries

4.3.3.5.2. 2-  flouride in oral enviroment provides remineralization of carious lesion it is posteruptive

4.3.3.5.3. 3- it has bacteriostatic effect ; it inhibits bacterial enzymes and stops its activites ; inhibiton of glucokinases

4.4. 4- Genetics

4.4.1. tooth morphology; inherited may have fewer fissures thus low caries susceptibility

4.4.2. familial enviromental habits; more important factor such as food habits and dental care

5. 2- Saliva

5.1. it is the medium in which bacterial plaque works ; thus have critical regulatory factor on caries

5.2. Role is

5.2.1. 1- Acquired enamel pellicle is formed by it; it initially protects enamel from colonizing bacteria

5.2.2. 2- Cleansing effect by flow of saliva; people with xerostomia have higher rate of caries, increased flow in mongolism decreases rate of caries

5.2.3. 3- Buffers in saliva ( carbonic acid/bicarbonate neutralize ph fall when bacteria metabolize sugar ; it is increases with increase flow

5.2.4. 4- Inorganic components as Fluoride Calcium Phosphate diffuse to plaque reducing enamel solubility and causes remineralization of caries

5.2.5. 5- Secretory IgA produced by plasma cell in salivary gland. its role is

5.2.5.1. killing bacteria

5.2.5.2. prevent its adherence to tooth

5.2.5.3. inhibit bacteria metabolic activity

5.2.6. 6-  lyzozymes, peroxides and lactoferrin have direct anti bacterial action

6. 3- Carbohydrates

6.1. importance

6.1.1. main compnent of diet upon which oral bacteria can act and produce acid

6.2. Factors contributing in cariogenecity of CHO

6.2.1. 1- Type of CHO

6.2.1.1. Monosaccharides: Glucose and Fructose

6.2.1.2. Disaccharide: Sucrose and Maltose and Lactose

6.2.1.3. 1- Sucros is considered the arch ciminal as

6.2.1.3.1. 1- most frequently consumed CHO

6.2.1.3.2. 2- Low molecular weight and can diffuse rapidly into dental plaque

6.2.1.3.3. 3- Consist of glucose, which will be utilized in formation of dextran, Dextran is glucose plymer, water insoluble and adhesive

6.2.1.3.4. 4- fructose which forms levan

6.2.1.4. 2- Polysaccharides: Starch and glycogen

6.2.1.4.1. little or no importance in etiology of caries

6.2.1.4.2. as people eating large amount of polysaccharides as rice in china and cereals in africa show less progress of caries

6.2.1.4.3. as they are of large molecular weights and don't diffuse readily into plaque

6.2.2. 2- Total amount of CHO

6.2.2.1. increase intake of fermentable carb is followed by little increase in caries activity

6.2.2.2. reducing sugar consumption on caries during war time ( world war II)  had slight decrease in caries incidence

6.2.3. 3- Frequency of CHO intake

6.2.3.1. ingestion of carb ar intervals between meals increase caries activity because

6.2.3.1.1. 1- CHO are present for longer time in the oral cavity increase period of activity of micro organisms

6.2.3.1.2. 2- cleansing effect of fibrous element is decreases

6.2.4. 4- Consistency and texture of CHO

6.2.4.1. sticky carbs are more cariogenic as they are slowly washed by saliva and remain for longer time thus more acid is produced

6.2.4.2. sollutions of sugar are quickly cleared thus causes less caries

6.2.4.3. dried powdered milk is sticky and highly cariogenic

6.2.4.4. liquid milk is not sticky and less cariogenic

6.2.5. 5- Refinement of CHO

6.2.5.1. industrial treatment of CHO to render them white, remove fibrous material and improve flavour

6.2.5.1.1. increase caries because

6.2.5.2. Honey is not refined but highly cariogenic

6.3. Vipeholm experiment

6.3.1. Gustafson made this experiment on 400 adult in mental hospital in Vipelhom city

6.3.2. aim was to investigate effects of total cho intake , frquency and texture and consistency on caries incidence

6.3.3. Divided patient into 7 groups all will low CHO diet

6.3.3.1. 1- 1 control group supplemented with caloric intake from margarine

6.3.3.2. 2- 2groups took sugar at mealtime in solution or sweetened bread

6.3.3.3. 3- 4 groups recieved sweets as toffees, caramels and chocolates between meals

6.3.4. Experiment conducted over 5 years 1946-1951

6.3.5. Observation from diagram

6.3.5.1. 1- eating sticky food as toffe and caramel between meals have highest caries activity

6.3.5.2. 2- effect of chocalate is less

6.3.5.3. 3- sugar in either form at mealtime showed little effect

6.3.5.4. 4- caries fell to its original low level when toffe and caramels stopped

6.3.5.5. 5- caries activity was very low in control group recieving low basic carb diet

6.3.6. Conclusion

6.3.6.1. 1- frequency of adminstration of CHO and texture of CHO showed greater effect on caries activity

6.3.6.2. 2- Total CHO intake showed little effect on caries activity

7. 4- MicroOrganisms

7.1. 1- Miller Experiment

7.1.1. miller was 1st to suggest that caries might be caused by action of bacteria on fermentable carbs

7.1.2. he suspended  2 sound teeth in 2 test tubes both with saliva and carbs

7.1.3. he boiled content in 1 tube and incubated thme at 37 degree

7.1.4. only tooth in the test tube not boiled suffered caries

7.1.5. concluded that boiling was bectericidal and therefore no caries occured

7.2. 2- Orland's experiment

7.2.1. confirmed conclusion of miller

7.2.2. obtained germ free rats by caeserian operation under aseptic conditons and breaded them for several generations in aseptic incubators

7.2.3. rats remained caries free despite feeding them highly cariogenic diet

7.2.4. then he created Gnotobiotic rats

7.2.4.1. with certain strain of micro organism introduced

7.2.4.2. they helped sort out the specied involved in dental caries

7.3. Characteristic of Cariogenic bacteria

7.3.1. 1- ability to produce acid from fermentable carb ( acidogenic property) enough to drop ph level below critical 5.5 causing demineralization of enamel and beginning of caries

7.3.2. 2-  can live, metabolize and grow and flourish in high acidic media ( aciduric property )

7.3.3. 3- synthesis of extracellular polysaccharide Dextran and leven to produce both pit and fissure caries and smooth surface caries

7.3.4. 4- Synthesis of intracellular polysaccharide ( amylopectin)

7.3.4.1. resembles starch and formed of glucose units

7.3.4.2. used by micro organism at time of diet insufficency

7.3.5. 5- attachment mechanism for firm adhesion to surface and each other

7.4. Types of Bacteria involved in caries

7.4.1. 1- Acidogenic

7.4.1.1. strept: viridans group

7.4.1.1.1. s. mutans

7.4.1.1.2. st. sanguis

7.4.1.1.3. st. mitis

7.4.1.2. Lactobacilli : L. acidophilus

7.4.2. 2- Proteolytic

7.4.2.1. 1- Actinomyces

7.4.2.2. 2- Clostridia

7.4.2.3. 3- Pseudomonas

7.4.3. Role of Strept

7.4.3.1. strept mutans were found to be potent cariogenic specially in smooth surface of teeth

7.4.3.2. charachters

7.4.3.2.1. 1- Powerful acid producer ( acidogenic ) readily ferment mon and disaccharide producing acid ( mainly lactic but also pyruvic and acetic )

7.4.3.2.2. 2- highly aciduric capable of living growing and metabolizing in high acidic media

7.4.3.2.3. 3- capable of producing smooth surface and pit and fissur ecaries due to ability to synthesis`e extracellular polysacharide dextran and Leven

7.4.3.2.4. Dextran is important as they are adhesive sticky substances enabling MO to adhere to smooth surface and other MO increasing amouth of bateria on surface and amoutn of acids produced

7.4.3.2.5. synthesise intracellular polysacharide amylopectin that act as store to be used at cho defiency

7.4.3.2.6. Other strpt

7.4.4. Lactobacilli

7.4.4.1. acidogenic

7.4.4.2. 2nd group associated with dental caries

7.4.4.3. were regarded as main cause of caries because they are present in large numbers in saliva and could be isolated from carious cavities

7.4.4.4. were used as index of caries activity

7.4.4.5. both acidogenic and aciduric

7.4.4.6. increase in number is probably a secondary phenomenon as their proliferation is favored by acidic enviroment

7.4.4.7. can not synthesize extracellular polysaccharide necessary for plaque formation thus can only produce pits and fissure caries

7.4.4.8. they have been isolated from carious dentin and are pioneers in dentin caries

7.4.4.9. have role in caries progression

7.5. Theories of Dental caries

7.5.1. 1- Acidogenic theory

7.5.1.1. millers theory ( chemicoparasitic theory

7.5.1.1.1. acidogenic bacteri feed on carbs producing bacteria mainly lactic acid

7.5.1.1.2. acid demineralizes inorganic part of enamel

7.5.1.1.3. proteolytic bacteria digest aorganix matrix of dentine

7.5.2. 2- Proteolytic theory

7.5.2.1. proteolytic bacteria act on organic matrix producing sulphuric acid demineralizing enamel

7.5.2.1.1. points agaist

7.5.3. 3- Proteolytic - Chelation Theory

7.5.3.1. proteoltic bacteria act on organic matrix liberating chelating agents demineralizing enamel

7.5.3.1.1. against

8. 5- Dental Plaque

8.1. 1. Definiton

8.1.1. tenaciously adherent biofilm

8.1.2. composed of bacterial structure accumulated on tooth surface

8.1.3. contain large number of closely packed micro organisms surrounded by extracellular material of bacterial and salivary origins

8.2. 2. Composition

8.2.1. 1- MO

8.2.1.1. 60-70% by volume mainly strept, lactobacilli and filamentous

8.2.2. 2- Matrix

8.2.2.1. 30-40% by volume composed of

8.2.2.1.1. proteins: glycoproteins, immunoglobulin enzymes as amylase and some epithelial cells

8.2.2.1.2. protein components are derived from saliva, gingival fluid and bacteria themselves

8.2.2.1.3. Carbs

8.2.2.1.4. Lipids

8.2.2.1.5. inorganic content:

8.2.2.2. Role of plaque matrix

8.2.2.2.1. 1- retains lactic acid in high conc. at particular site where it can initiate caries ( Diffusion Limiting Membrane )

8.2.2.2.2. 2- Slows down entry of buffers from saliva thus delaying neutralizing action ( Diffusion limiting membrane

8.2.2.2.3. 3- increases resistance of plaque to be washed away from the tooth and contributes to its adhesivenes and bulk

8.3. 3. clinically

8.3.1. plaque is seen when tooth brushing is stopped for 12-24 hr and it is covered by transparent film dulling enamel shiny surface

8.3.2. increase thickness of plaque, becomes visible by naked eye can be detected by disclosing

8.3.3. self cleansing forces can not remove plaque but decrease its thickness

8.3.4. entire removal is chieved by brushing and flossing

8.3.5. great amount of plaque is found in stagnation areas as interproximal areas, gingival margins and deep fissures

8.3.6. forms rapidly and in great thickness and amount on high sugar diet

8.4. 4. Types

8.4.1. supragingival Plaque: Dental plaque located at tooth surface above gingival margin

8.4.2. supragingival Plaque: Dental plaque located at tooth surface above gingival margin

8.4.3. subgingival: located below gingival margin

8.4.4. both differ in composition and effects

8.5. 5. Interfaces of plaque

8.5.1. 2- Plaque saliva ready access to nutrients for bacterial growth

8.5.2. 3- plaque gingiva interface: bacteria at this site recieve nutritional input from gingival fluid and their matabolic end products affect gingival tissue in close proximity 2

8.6. 6. Mecheanism of formation

8.6.1. 1- Acquired enamel pellicle

8.6.1.1. acellular structure less bacteria free film of salivary glycoproteins

8.6.1.2. thickness is 0.3-1 micron formed immediately after tooth brushing

8.6.1.3. formed by selective adsorption of certain salivary glycoproteins to hydroxyapetie

8.6.1.4. composed of salivary glycoproteins which is a long core of protein attached to carbohydrate group

8.6.1.5. it also forms on artificial sufaces as restoration, orthodontic aplliances and denture

8.6.2. 2- Initial community

8.6.2.1. 1- Colonization phase (8hr)

8.6.2.1.1. The pioneer bacteria are st sanguis and st mitis and actinomysis viscosis

8.6.2.1.2. initial colonizers have surface components adhesions which bind to complementary molecules on pellicle by thread like extensions from surface of bacterial cell wall and sometimes the extension resemble glue like coat seen by electron microscope

8.6.2.1.3. some release extracellular enzyme which liberate carb group from pellicle glycoprotein and use them as source of energy

8.6.2.2. 2- Growth phase (8-48) hour

8.6.2.2.1. rapid growth result in formation of bacterial colonies

8.6.2.2.2. they coalesce with each other forming monolayer of organism covering pellicle

8.6.2.2.3. then bacteria proliferate in vertical direction perpendicular to tooth

8.6.2.2.4. then growth slows down and number of organisms remain constant after

8.6.2.3. 3- Intermediate community

8.6.2.3.1. starts with entrance of 2ry invaders ST MUTANS

8.6.2.3.2. increase in complexity of plaque is seen

8.6.2.3.3. Strept is inl large number and have 2 effects

8.6.2.4. 4- Mature Community

8.6.2.4.1. with maturation of plaque filamentous organism proliferate and predominate and are parallel to each other and perp to tooth

8.6.2.4.2. then wide variety of other strains of bacteria join plaque community as lactobacilli, actinomyces, diphteroids and others

8.6.2.4.3. bacterial aggregation CORN CUBS seen in EM. consisting of central filament covered by dense layer of coccal forms

8.6.2.4.4. differential microbial compositon varies from different persons

8.7. 7. Factors Affecting Cariogenecity Of plaque

8.7.1. 1- Amount and thickness of plaque

8.7.1.1. plaque not able to produce caries unless it attains certain thickness

8.7.1.2. thickness is affected by

8.7.1.2.1. 1- size and distribution of stagnation areas

8.7.1.2.2. 2- use of oral hygiene methods

8.7.1.2.3. 3- Functional mouth movements

8.7.1.2.4. 4- type of Carb consumed

8.7.2. 2- type of bacteria in plaque

8.7.2.1. whether plaque will be involved in periodontal disease or caries process

8.8. 8. Stephan's Curves ( Acid production in plaque )

8.8.1. experiment aimed to study changes in PH of plaque after glucose intake

8.8.2. Bacteria ferment mon and disaccharides to produce energy for bacteria and organic acid mainly lactic responsible for initiation of dental caries

8.8.3. electrode is in contact with plaque to measure ph changes another in floor of mouth to measure resting PH one hour after meal when there was no fermentable carb in oral cavity

8.8.4. patient were allowed to rinse mouth with 25ml 10% glucose sol for 10 seconds then spit or swallow

8.8.5. ph changes where recorded frequently and ph valuse plotted

8.8.6. Results

8.8.6.1. after glucose rinse ph drops rapidly reaching critical ph 5.5 in 2-5 minutes depending on caries activity of pateints

8.8.6.2. ph remains under critical level for 10-30 minutes depending on caries activity

8.8.6.3. ph slowly return to resting ph after one hour

8.8.6.4. Ph drops rapidly due to

8.8.6.4.1. 1- rapid diffusion of sugar into dental plaque

8.8.6.4.2. 2- presence of large numbers of active bacteria and their enzymes in plaque

8.8.6.5. PH returns slowly due to

8.8.6.5.1. 1- persistant metabolism of residual sugar

8.8.6.5.2. 2- breakdown of stored polysaccharide in plaque

8.8.6.5.3. 3- diffusion limiting property of plaque delay entry of buffers and exit of acid

8.8.6.6. when sucrose or fructose is used similar curve is produced

8.8.6.7. non fermentable carbs as xylitol caused no drop in pH of plaque

8.8.6.8. polysaccharides causes no drop in ph ( high molecular weight)

8.8.6.9. in normal life person may not wait till ph return to normal and continues to consume sweets so ph continue to drop more and more

8.9. 9. Biochemical reactions of dental plaque

8.9.1. 1- Acid production in dental plaque (stephan's)

8.9.2. 2- Formation of extracellular polysaccharides (dextran and leven)

8.9.3. 3- Formation of intracellular polysaccharide amylopectin

8.9.4. 4- Demineralization pase

8.9.5. 5- Remineralization phase

9. Pathology of Dental Caries - Enamel Caries

9.1. 1- Macroscopic appearance:

9.1.1. Early smooth surface caries appear as opaque chalky white ( white spot)

9.1.2. arrested or slowly progressing lesion appear as brown spot

9.1.3. may become rough to probe and later on cavitation occurs

9.1.4. pit and fissure caries appears as opaque bordered zone related to fissure periphery and may be stained brown

9.2. 2- xray picture

9.2.1. proximal surface caries appear as cone shaped radiolucent area in enamel with intact outer surface

9.3. 3- Histopathological appearance:

9.3.1. findings of enamel caries are domstrated on longitudinal ground sections and have been examined by:

9.3.1.1. Polarized light microscope

9.3.1.1.1. determines percent of enamel pores by volume

9.3.1.2. Ordinary light microscope (transmitted light)

9.3.1.2.1. using a mounting medium as canada balsam having same refractive index as enamel

9.3.1.3. Microradiography:

9.3.1.3.1. small x ray film placed in contact with ground section and exposed to xray

9.3.1.3.2. this microradiofraphy reflect the amount and distribution of minerals

9.3.1.4. Chemical analysis

9.3.1.4.1. chemical structure is studied for seperate zones obtained by microdissection

9.4. Smooth surface caries

9.4.1. early smooth surface caries white spot lesion

9.4.2. caries is cone shaped with base toward enamel surface and apex toward DEJ

9.4.3. lesion due to action of acids resulting in submicroscopic pores

9.4.4. in ground section it consists of 4 zones

9.5. Pits and fissure caries

9.5.1. in early stages it has histological zones similar to smooth surface caries

9.5.2. shape of lesion differs bacause of different angulation of enamel rods

9.5.3. lesion start as 2 cones with their bases on lateral surface of fissure and later they coalesce to form one cone at depth of fissure

9.5.4. since enamel is thinner at base of pits and fissure lesion progress at a fast rate than smooth surface

9.6. Zones of early enamel lesion:

9.6.1. 1- Initiation Phase

9.6.1.1. Translucent zone

9.6.1.1.1. located on advancing front of lesion toward dentine it is the first observed changes histologically in early caries

9.6.1.1.2. by polarized light : appears to be due to formation of pores 1% of total Enamel volume; normal contain 0.1%

9.6.1.1.3. By transmitted light: zone appears translucent because mounting media canada balsam have same refractive index as enamel so when pore become filled with it the normal structural features is lost and zone appear translucent

9.6.1.1.4. Microradiography

9.6.1.1.5. Chemical analysis

9.6.1.2. Dark zone

9.6.1.2.1. lies superficial to translucent zone

9.6.1.2.2. by polarized light : increase in volume of pores, some small and some large. spaces are about 2-4% of enamel volume

9.6.1.2.3. additional spaces caused by smaller pores formed in addition to those in translucent

9.6.1.2.4. smaller zones may be due to reminelarization in large pores when there is no acid production

9.6.1.2.5. By transmitted light: brown or dark because smaller pores are smaller than to allow canada balsam in and air fills it instead and light is scattered causing brownish color

9.6.1.2.6. Microradiography

9.6.1.2.7. Chemical analysis

9.6.1.3. Body of the lesion

9.6.1.3.1. largest zone beneath surface of dark zone

9.6.1.3.2. by polarized light : increase pores representing 5-25% of enamel volume 5% at periphery and 25% at center

9.6.1.3.3. By transmitted light: radiolucent compared with sound enamel and sharply demakated from dark zone

9.6.1.3.4. striae of retzius demonstrated in this lesion

9.6.1.3.5. Microradiography

9.6.1.3.6. Chemical analysis

9.6.1.4. Surface zone

9.6.1.4.1. surface zone is 30 micron

9.6.1.4.2. represent feature where surface zone remain intact while demineralization occur at subsurface level

9.6.1.4.3. by polarized light : decrease in volume of pores

9.6.1.4.4. By transmitted light: dark

9.6.1.4.5. Microradiography

9.6.1.4.6. Chemical analysis

9.6.1.5. clinically its a white spot lesion

9.6.1.6. may become stained by pigment from food tobacco or bacteria then called brown spot

9.6.2. 2- Phase of Bacterial Invasion

9.6.2.1. sufficient spaces created by acid bacteria starts invasion

9.6.3. 3- Phase of Destruction

9.6.3.1. proteolytic bacteria act on organic matrix leading to complete destruction of area

9.6.4. 4- Phase of 2ry enamel caries

9.6.4.1. caries reaches DEJ spreading laterally

9.6.4.2. enamel bocme undermined giving bluish white appearance

9.6.4.3. extension along DEJ may result in 2ry caries attack of enamel from beneath

9.6.5. time of caries progress through enamel on proximal surface of permenant teeth takes month to years depending on cariogenic properties

10. Dentin Caries

10.1. 1. Macroscopic picture

10.1.1. outline is cone shape with base at DEJ and apex toward pulp

10.1.2. dentin is brownish and soft to probe

10.2. 2. Microscopic Picture

10.2.1. 1- Initial uninfected lesion ( prior to cavitation of enamel)

10.2.1.1. advancing front of enamel caries have reached dej but enamel surface is intact and no cavity formed

10.2.1.2. zones

10.2.1.2.1. 1- zone of reactionary or reparative dentine

10.2.1.2.2. 2- zone of sclerotic or translucent dentine

10.2.1.2.3. 3- Body of lesion

10.2.2. 2- infected lesion

10.2.2.1. after bacterial invasion of enamel and formation of enamel cavity.

10.2.2.2. dentinal tubules provide pathway for invasion of dentine by bacteria

10.2.2.3. organsims form 2 waves:

10.2.2.3.1. 1- pioneer organsims: at front of lesion consist of acidogenic bacteria and decalcify matrix

10.2.2.3.2. 2nd wave of mixed infection with proteolytic bacteria which distorts the matrix

10.2.2.3.3. zones: