Dental Caries Handout PDF

Dental Caries Definition: Dental caries is a progressive microbial disease affecting susceptible hard tooth structures characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth. Etiology of Dental Caries -Contributing etiologic...

Dental Caries Definition: Dental caries is a progressive microbial disease affecting susceptible hard tooth structures characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth. Etiology of Dental Caries -Contributing etiological factors to dental caries: 1- Cariogenic Bacteria (Agent) 2- Substrate (Fermentable Carbohydrate) 3- Susceptible Tooth and Saliva (Host) 4- Time 5- Means of localization of micro-organisms and substrate at site of attack on tooth surface (dental plaque). 1- CARIOGENIC BACTERIA Role of bacteria in dental caries: Cariogenic bacteria produce acids (resulting from fermentation of carbohydrates) that lead to demineralization of enamel and dentin. 1 Experiments to Demonstrate the Role of Cariogenic microorganisms in Caries Development:  Miller’s Experiment: Miller’s work revealed that caries-like lesions were produced by incubating teeth in saliva when carbohydrates were added. He was the first to suggest that caries process result from the fermentation of carbohydrates by the bacteria present in saliva. The resulting acid lead to demineralization of enamel and dentin.  Orland’s Experiment: a- Production of Germ-free animals: Aim: Is bacteria essential for production of dental caries? - A pregnant female rat was put in a sterile operating theatre to deliver her off springs under complete aseptic conditions. - A caesarian section was done, and the delivered rats were divided into two groups; a group was left in the aseptic conditions and the other group was placed outside under ordinary life conditions -Then, both groups were fed a cariogenic diet. The rats were kept under close observation to identify any caries development. Results: The group that was kept under aseptic conditions (germ free rats) did not produce dental caries when compared to their siblings under normal life conditions. Conclusion: Bacteria is essential for production of dental caries. 2  b- Production of Gnotobiotes: Gnotobiote: known life Aim: - Which bacteria produces dental caries? - Which type of caries is produced by each type of bacteria? After the production of germ-free rats, they were divided into groups and fed cariogenic diets with one known strain of micro-organism (streptococci, staphylococci, lactobacilli, actinomyces, etc.). Results: - After a period of time, the rats given the diet with streptococcus mutans produced smooth surface and pit and fissure caries. - The group that was fed cariogenic diet with lactobacilli produced pit and fissure caries only. - The other groups didn't produce dental caries. Conclusion: 1- Not all bacteria produce dental caries. 2- Streptococcus mutans is more cariogenic than lactobacilli. 3  What are the Essential Features for a Bacteria to be Cariogenic? 1. Ability to produce acids = Acidogenic 2. Ability to survive in an acidic environment = Aciduric 3. Synthesis of insoluble extracellular polysaccharides glucans (dextrans) and (levan) Dextran afford a means of adhesion to smooth tooth surfaces and form the bulk of dental plaque. They also act as a barrier to the diffusion of acids from the plaque and the entry of salivary buffers into plaque 4. Synthesis and utilization of intracellular storage polysaccharides (amylopectin) Amylopectin reserve fermentable carbohydrate after dietary carbohydrate has been cleared away 5. Ability to actively transport fermentable sugars when in competition with other plaque bacteria even against a concentration gradient 6. Have attachment mechanisms for firm adhesion to tooth surfaces 4 CARIOGENIC BACTERIA 1) Streptococcus mutans Able to ferment a variety of sugars, i.e. they are acidogenic Very acid tolerant; can live at a low pH of 4.2 (aciduric) Closely associated with the initiation of caries in humans. This is attributed to the organism’s ability to synthesize extracellular polysaccharides dextran and levan. Dextrans, are insoluble and adhesive sticky substances enabling micro-organisms to adhere to smooth tooth surface and to other microorganisms (i.e. having attachment mechanisms). Levan is used as a storage for carbohydrates. They are capable of producing intracellular polysaccharides (amylopectin) It adheres to plaque pellicle by Adhesins Named mutants because of its varying morphology. They undergo mutation in their morphology by changing their shape from round to rod under different environmental conditions like decrease in pH. They are transmissible from one individual to another 2) Lactobacillus species 1. Acidogenic 2. Aciduric can live at a low pH of 5.4 Lactobacilli are capable of producing pit & fissure caries only in gnotobiote animals. They can’t produce extracellular or intracellular polysaccharides thus they cannot attach themselves to the smooth surfaces of the teeth. They do not play an important role in the initiation of dental caries, though they play a role in its progression. 5  They have been isolated from carious dentin and are considered as pioneer organisms in dentin caries The lactobacilli count was once used as an index of caries activity as it was observed that lactobacilli are present in large numbers in saliva in persons with high caries activity. 2. Role of Fermentable Carbohydrates (Substrate) in Dental Caries Factors affecting cariogenicity of carbohydrates: a- Types of carbohydrates: -Monosaccharides: glucose and fructose - Disaccharides: sucrose, maltose and lactose - polysaccharides: starch and glycogen -Disaccharides are the most cariogenic carbohydrates, sucrose, in particular, has been described as the arch criminal of dental caries. This is because: 1- Sucrose is cheap, available in many forms and most frequently consumed carbohydrate 2- It is of low molecular weight and can thus diffuse rapidly into dental plaque 3- Sucrose is rapidly broken down by bacterial enzymes to produce acids. 4- The energy liberated from the break of the disaccharide bond is used by cariogenic bacteria to produce dextran and levan. Sucrose with the help of cariogenic bacteria (S.mutans) plays an active role in building of bacterial plaque forming extracellular polysaccharides. 6  Hydrolysis Glycolysis Invertase Glucokinase Organic Acid+ Glucose H2O+Energy Sucrose Organic Acid+ Fructose H2O+Energy Fructokinase Glucosyltransferase Glucose Dextran Sucrose Fructose Levan Fructoosyltransferae 7 What's the difference between Dextran and Levan? Polysaccharides (starch, glycogen and cellulose) are less cariogenic because: 1- They are of high molecular weight and can’t diffuse rapidly into plaque 2- Not easily metabolized by oral bacteria; since breaking down of polysaccharides into simple sugars by amylase in the saliva is a slow process. b- Total Amount of Carbohydrate Intake ↑↑ Amount of CHO intake → ↑↑ caries activity ↓↓ Amount of CHO intake → ↓↓caries activity c- Frequency of Intake of Carbohydrate Frequent intake of CHO, increases caries susceptibility because: 1- Increased periods of availability of the CHO in the oral cavity leading to increased periods of micro-organisms activity producing more acids. (Low pH) leading to more acid demineralization to tooth structure 2- Cleansing effect of other fibrous food elements is absent. 3-No chance for pH to return to normal as the pH takes a long time to return to normal after carbohydrates intake (Stephan’s curve). 8  d- Texture of carbohydrate: Sticky carbohydrate is more cariogenic because: It remains for a long time in the oral cavity in relation to tooth surface and it is slowly washed by saliva so it is more accessible to micro- organisms for a longer time to produce more acids e- Refinement of Carbohydrate: Definition: It is the treatment of raw carbohydrate (e.g. sugar cane) in industry to produce a refined sugar that is: -whiter -sweeter -less fibrous material - Better flavor Refinement of carbohydrates increases cariogenicity because: 1- Increase concentration of fermentable fraction of carbohydrate 2- Increase adhesiveness 3- Removal of fibrous material -Xylitol is refined but non/anticariogenic due to its lack of suitability for microbial metabolism (nonfermentable). -Honey is highly cariogenic although it’s not refined 9 Experiment to demonstrate the role of CHO in caries development: Vipeholm Experiment: Aim: To investigate the effect of: a) Amount, b) frequency of intake c) texture of carbohydrates (stickiness) on dental caries susceptibility The experiment was conducted in Vipeholm Hospital which is an institute for the mentally deficient in Sweden. A total number of 436 patients were divided into 7 groups according to the diet given -Control group received a basic low CHO diet supplemented to adequate caloric intake by fat. - Two groups took sugar at meal times either in solution or as sweetened bread. - Four groups received sweets in form of toffees, caramels or chocolates between meals.  Results: A) Eating sticky carbohydrates as toffees and caramels between meals showed the highest caries activity. B) The effect of chocolates were less severe. C) Sugars, in either form at meal times showed little effect on caries. D) Caries activity was very low in the control group receiving the low basic carbohydrate diet.  Conclusion: 1- Frequency and texture of CHO are more effective on caries activity than total amount. 2- Sugar in a form that is retained on the teeth (sticky) or eaten at frequent intervals must be regarded as the most potent cause of dental caries. 10  3.Dental plaque Definition: Dental plaque is a tenacious bacterial structure formed on tooth surfaces. It is formed of a diverse community of closely packed bacteria embedded in a matrix. Dental plaque is a structurally and functionally an organized BIOFILM. Composition: Micro-organisms (60-70% by volume) An amorphous matrix (30-40% by volume) Composed of: -Proteins (derived from saliva, gingival fluid) -Carbohydrates (dextran, levan, amylopectin) -Inorganic content (Ca, P, F) Role of plaque matrix: 1. Acts as a diffusion-limiting membrane: a. retain the produced organic acid (lactic acid) in high concentrations to initiate caries activity b. slows down the entry of buffers from saliva to delay their neutralizing action 2. Contributes to adhesiveness, bulk and resistance to washing by saliva Factors affecting plaque formation and thickness: 1. Anatomy and position of tooth 2. Presence of appliances 3. Structure of tooth surface 4. Friction from the diet and masticatory movements 5. Oral hygiene measures 6. Composition of the diet 11 Mechanism of formation of Bacterial Plaque 1) Formation of an acquired enamel pellicle 2) Colonization of cell-free pellicle by bacteria (formation of dental plaque) a. Initiation of a pioneer community b. Formation of an intermediate community c. Establishment of a mature community 1) Formation of an acquired enamel pellicle: Definition: An acellular, structureless, organic, bacteria-free film of salivary glycoproteins on enamel surface formed by selective adsorption of specific salivary glycoproteins through electric charges found on the apatite crystal. Acquired enamel pellicle is 0.1-1.0 μm thick. The natural development of a pellicle is intended to protect the teeth from acids. Pellicle acts as a diffusion barrier, slowing both attacks by bacterial acids and loss of dissolved calcium and phosphate ions. However, it also provides a means for bacteria to latch onto the teeth. So rather than attaching to minerals within teeth, microbes adhere to the pellicles. 2) Colonization of cell-free pellicle by bacteria: I. Initial Community 1- Colonization phase (8 hours): Primary colonizers (pioneers): S.sanguis, and Actinomyces viscosus 2- Rapid growth phase (8-48 hours): bacteria spread as a monolayer and then palisade perpendicular on the tooth surface II. Intermediate Community (Secondary colonizers) – Strep. mutans attach to the established pioneer species via adhesin-receptor interactions - Acid production - Formation of extracellular poly saccharides (Dextran and Levan) – So selective replacement happens within the plaque flora as follows: 12  1. Aciduric organisms will flourish (Veillonella and S. mutans) → positive interaction; and those which are less aciduric will disappear (S. sangius) → negative interaction. 2. Aerobic species in the deeper layers are replaced by anaerobic ones. Microbial succession is a dynamic process involving continuous replacement of the microbial communities according to the new environmental conditions III. Mature Community (2weeks or older) Filamentous organisms proliferate and predominate arranging themselves parallel to each other and at right angles to the tooth surface. This arrangement of distinctive bacterial aggregations is referred to ‘corn on the cobs’. By this time a wide variety of organisms join the community including lactobacilli, actinomyces. Biochemical Reactions Occurring in Bacterial Plaque 1- Acid production (Stephan’s experiment) 2- Formation of extracellular polysaccharides 3- Formation of intracellular polysaccharides 4- Demineralization phase 5- Remineralization phase Stephan’s Experiment: Aim: To study the changes occurring in the pH of plaque after glucose intake. - He divided individuals into groups according to caries activity. - pH was recorded after two hours of the last meal (on a day during which no fermentable carbohydrates were consumed) and this pH is called resting pH - One micro-electrode was placed in contact with the developed plaque on teeth and another was placed in the floor of the mouth (saliva the electrolyte medium) 13  - Individuals were asked to rinse their mouth for ten seconds with 25 ml. of 10% glucose - After two minutes, the pH was recorded immediately, after 5 min. and then every 10 min. - The pH values were plotted against time and a curve was produced called Stephan's curve Results: 1- The curves show that after the glucose rinse in the pH drops rapidly reaching the critical pH.(5.5) within 2-5 minutes ( depending on the caries activity of the patients). The pH remains under the critical level for 10-30 minutes (depending on caries activity). Then the pH returns slowly to the resting pH level after one hour. The rapid fall in the pH is due to: a- Rapid diffusion of sugar into dental plaque b- The activity of large numbers of bacteria and enzymes in the dental plaque The slow return in pH is due to: a- The continued metabolism of residual sugar absorbed by the plaque. b- The breakdown of reserve polysaccharides in the plaque c- The diffusion limiting property of dental plaque resulting in: i. Delayed diffusion of salivary buffers into the plaque ii. Delayed diffusion of acids outward into the saliva 2- The caries susceptible patients (C.S.P) show a lower fall in pH which remains for a longer time below the critical level compared to the caries resistant patients (C.R.P). so the more time below the critical pH the more is the caries activity 14 C.R.P C.S.P In normal life the individual may not wait until the pH of his mouth returns to the resting level but he continues to consume sweets or fermentable CHO so the pH continues to drop more and more and further caries is produced. Demineralization and Remineralization Dental caries is a dynamic process. It consists of periods of demineralization and periods of remineralization. Remineralization occurs when the sugar intake stops, and the oral hygiene is established by good tooth brushing. When the periods of demineralization exceed those of remineralization then caries is produced. When the periods of remineralization are more than the periods of demineralization, the lesion becomes resistant and arrested caries is produced. 15  4.Host Factors a) Susceptible Tooth: i. Position: - Upper or lower teeth? - Posterior or anterior teeth? - Properly aligned or malposed / crowded teeth? ii. Morphology: Pits and fissures are much more susceptible to caries than the smooth tooth surface. This is because they are more difficult to clean. Their shape and depth determine the degree of caries susceptibility. Deep and narrow pits and fissures are more prone to decay than wide and shallow pits.  V type and U type fissures are more caries resistant that I type and Y type.  Contact areas: point contact (in young patients) are more caries resistant than board contacts (in old patients) which are characterized by more food retention and stagnation. iii. Structure: Enamel hypoplasia and enamel hypo calcification mat affect the rate of progression but not the initiation of caries Newly erupted teeth are more caries susceptible, but later, the resistance of these teeth to caries increase due to post eruptive maturation which occurs due to hyper mineralization and increase fluoride content of enamel surface. iv. Fluorides: The increase in fluoride content in tooth increases its resistance to dental caries. (cariostatic) 16  Fluoride supply: Water which should not exceed 1.5 parts per million (during development). Drinks as tea Food as seafood Therapy as topical application of fluoride (after eruption). Mechanism of action of fluoride: Three main actions: 1- Increasing enamel resistance to demineralization: Fluoride replaces the hydroxyl group in the hydroxyapatite forming fluorapatite which is less soluble in acids. 2- Enhances remineralization. 3- Inhibits bacterial growth: Fluoride inhibits bacterial enzymes v. Genetic Factors Favorable or unfavorable tooth morphology is genetically inherited. Environmental factors as food habits and regular dental care acquired from family have more effect then genetic factors. b) Saliva The role of saliva in dental caries could be summarized as follows: 1- Specific salivary glycoproteins from the acquired enamel pellicle which initially protects the enamel surface from being colonized by oral bacteria. 2- The flow of saliva has a cleansing effect on the mouth and teeth. Human beings suffering from lack of salivary secretion (Xerostomia) usually show increased rate of dental caries. 3- Salivary buffers (mainly carbonic acid/ bicarbonate system) can neutralize the pH fall (acidity) which occurs when plaque bacteria metabolize sugar. The buffering capacity of saliva is increased with higher rates of salivary flow. In mongolism decreased caries incidence 17  may be due to increased rate of salivary flow with its associated buffering elements. 4- The inorganic components of saliva (calcium, phosphate and fluoride) diffuse into the plaque reducing the solubility of enamel and promoting the remineralization of the caries lesion 5- Saliva contains secretory immunoglobulin A (sIgA) which is produced by plasma cells found in salivary glands, the main role of sIgA is killing of bacteria, prevention of adherence of bacteria and inhibition of bacterial metabolic activity. 6- Anti-bacterial substances in saliva have direct anti-bacterial action on plaque action on plaque microorganisms (such as lysozyme, lactoferrin and peroxide) PATHOLOHY OF DENTAL CARIES I. Macroscopic Appearance Appear as an opaque chalky white area ‘white spot’ (initial enamel caries) II. Microscopic Appearance 1- Histopathology of Enamel caries: Permeation of enamel by acids cause a series of submicroscopic changes (pores). Process of enamel caries is a dynamic one since the initial lesion consists of alternating phases of demineralization and remineralization rather than a continuous process of dissolution. Enamel caries develops in four main phases: i Phase of initiation (initial enamel caries) ii Phase of bacterial invasion iii Phase of destruction iv Phase of secondary enamel caries 18 Methods to identify initial Enamel Caries: (longitudinal ground section) 1. Ordinary light microscope depends on Canada balsam or Quinoline (mounting medium) having same refractive index as enamel (RI=1.62) 2. Polarized light microscope determines % of enamel pores by volume. 3. Microradiography reflects the amount and distribution of minerals present by black and white. 4. Microhardness testing measures hardness value of the microscopic section. A) INITIAL ENAMEL CARIES:  The early enamel lesion (white spot) in smooth surface caries is cone shaped with the base of the cone on the enamel surface and the apex pointing towards the amelodentinal junction.  The shape of the lesion differs in pits and fissure caries showing 2 cones.  Submicroscopic pores are created by the diffusion of hydrogen ions.  - In ground sections the early smooth surface enamel caries lesion consists of four zones. 1- Translucent zone:  The first changes located on the advancing front of the lesion (i.e. towards dentin)  By transmitted light: this zone appear translucent because the mounting media used in the section (quinoline) have the same refractive index as enamel so when the submicroscopic pores become filled with it the normal structural features are lost and this zone appearance is translucent.  Microradiography: slight radiolucent  Submicroscopic pores account for 1% of total enamel volume  This zone represents initial demineralization. 19  2- Dark zone: Superficial to translucent zone Further demineralization takes place (nearer to the source of acid) The additional spaces are caused by smaller pores formed in addition to those seen in the translucent zone. It is believed that the smaller pores may be due to remineralization which occurs in the larger pores in periods when there is no acid production. By transmitted light: it appear dark because the smaller pores are so minute that the larger molecules of the quinoline don’t enter and air is allowed to pass instead and light is scattered causing the brownish color of this zone. Submicroscopic pores account for 2 - 4% mineral loss of total enamel volume Radiolucent compared to previous zone and to enamel 20  3- Body of the Lesion Largest zone extending beneath the dark zone and below the surface zone Increased pores, 5% (at the periphery) - 25% (at the center of the lesion) By transmitted light : appears translucent The striae of Retzius are well marked in this zone indicating preferential mineral dissolution along these areas of relatively higher porosity More radiolucent (alternating radiolucent and radio-opaque lines) Progressive demineralization. (most demineralization) 4- Surface Zone 25-30μ thick with decrease in pores. More radio-opaque than the deeper zones since it is more mineralized than the underlying body of the lesion. Surface remains intact because there is an increase concentration of minerals and fluorides on surface since caries is a dynamic process (alternating phases of demineralization and remineralization). The greater resistance of surface enamel zone is due to: a- The active reprecipitation of minerals derived from the plaque and from deeper layers of the lesion as dissolved minerals diffuses outwards. b- Higher fluoride content. Zone Comments Translucent zone Broader in progressing caries, narrow or absent in arrested or re-mineralized lesions. Dark zone Broader in arrested or re- mineralized lesions, narrow in advancing lesions. Body of the lesion Broader in progressing caries; replaced by a broad dark zone in arrested or re- mineralized lesion. Surface zone Relatively constant width; a little thicker in arrested or re-mineralizing lesions. 21  B) PHASE OF BACTERIAL INVASION:  When sufficient pathways are created by the action of acids, central defects occur to hollow the crystals.  As dissolution increases, disorganization of crystal arrangement occurs (pores become large enough after removal of sufficient amounts of minerals to allow the invasion of bacteria). C) PHASE OF DESTRUCTION:  Loss of enamel minerals leads to loss of structure (90% by volume) The structural integrity of enamel is lost The organic matter either collapses or is digested by the action of proteolytic bacteria (proteolytic enzymes) D) PHASE OF SECONDARY ENAMEL CARIES: When the acids reach the dentino-enamel junction (DEJ), it spreads laterally. This lateral spread gives enamel the bluish-white appearance seen clinically. Three major effects of the lateral spread: 1- Enamel loses support of dentin and hence it is weakened/ undermined (separation of enamel from dentine) 2- Reverse attack from beneath (secondary enamel caries) 2- Spread of acids followed by bacteria along DEJ which allows the attack of dentin over a wide area. 22  2- Histopathology of dentine caries: What is Dentine?  Mineral phase: about 75%  Organic phase: about 20%  Dentinal tubules forms the bulk of the matrix  Odontoblastic processes occupy the dentinal tubule to end by odontoblasts in the pulp (i.e living tissue) The initial (non-bacterial) lesion forms deep to carious enamel before any cavity has formed. Acids affect dentine before any cavitation of enamel occurs (irritation of odontoblast). The dentinal lesion involves: I- uninfected lesion (deepest and most close to the pulp) → Acid Attack II- infected dentinal lesion (bulk of the lesion) → Bacterial Invasion III- area of dentinal destruction I. Uninfected Dentinal Lesion (acid attack): 1- Zone of Fatty Degeneration: Acids reach dentine, irritate the odontoblastic processes in the tubules giving rise to a zone of fatty degeneration 23 2- Zone of Hypermineralization (Zone of Sclerosis): Superficially to this zone a zone of hypermineralization is observed. Source of minerals in this zone may be: 1- active transport by odontoblasts from blood via the pulp 2- passively from the minerals liberated from the demineralization process of the dentinal tubules’ wall This zone (peritubular hypermineralized zone) results in an increase in a calcified barrier by reducing or narrowing the diameter of the tubules against the acid attack and bacterial invasion thus protecting the odontoblastic layer and pulp Around and below this layer reparative dentin is laid down. It is a defense reaction of the pulp against the acid attack 3- Zone of Hypomineralization: (demineralized) With more acids the inner walls of the tubules become demineralized increasing the diameter of the tubules and becoming more distended. The end result of this zone is widening of the tubule making a pathway for the invading bacteria. II. Infected Dentinal Lesion (bacterial invasion): Develops after bacterial invasion occurs in enamel and a cavity is formed, i.e. surface of enamel is not intact Zone of bacterial invasion: 1. Pioneers: the first leading group of bacteria invading the dentin; usually acidogenic. 2. Beading: The progress of micro-organism pulpally does not proceed in a continuous manner but rather occurs in alternating active and resting phases. This results in the formation in separate and distinct aggregates within dentinal tubules separated by segments that are free from micro-organisms. 3. Liquefaction foci and transverse clefts: further proliferation of the microorganisms within the dentinal tubules results in adjacent beads coalescing with each forming larger distended segments of dentinal tubules filled with 24  microorganisms and necrotic debris. Liquefaction foci are longitudinal in orientation, while transverse clefts are perpendicular to the dentinal tubules. Transverse clefts are similar to the liquefaction foci in their content and are formed due to spread through: 1- lateral branches of the dentinal tubules 2- along the incremental lines The bacterial invasion occurs in two waves: 1) The first wave consists of acidogenic organisms (pioneers). 2) The second wave, mixed acidogenic and proteolytic organisms. Infected Dentinal Lesion Uninfected Dentinal Lesion Bacteria is involved after widening of No bacteria is involved, acid attack dentinal tubules and softening only Not remineralizable and should be Remineralizable and should be removed preserved Zones : Zones: -Pioneers - Zone of Fatty Degeneration: -Beading - Zone of Hypermineralization: -Liquefaction foci and transverse clefts - Zone of Hypomineralization: (demineralized) 25 26 III. Area of dentinal destruction (superficial zone):  Neighboring liquefaction foci and transverse clefts coalesce with each other forming progressively larger and more irregular cavities filled with micro- organisms and debris. Fatty degeneration 27 Root surface caries: Usually due to exposure of the neck of the tooth to the oral environment as a result of gingival recession (periodontal diseases or age changes). The exposed enamel-cementum junction is highly irregular and presents a bacterial retention site. In contrast to early enamel caries the bacteria in the plaque on the root surface penetrate into the superficial layer of the demineralized cementum very early invading it along the exposed collagen fibers (Sharpey’s fibers). The basic reactions and carious destruction of root dentine is similar to that described for coronal caries. Likewise, reactive dentine is formed towards the pulp corresponding to the involved tubules. Reactionary changes in Dentin 1- Tubular sclerosis (translucent dentin): Peritubular dentin decreases size of dentinal tubules against the acid attack and bacterial invasion. 2- Dead tract: In case of a severe stimulus, Death of odontoblasts occur leaving empty dentinal tubules which appear dark in transmitted light. 3- Regular reactionary dentin: Mild stimuli by caries = dentin formed with tubular structure at the dentin pulp interface. 4- Irregular reactionary dentin: Moderate to severe stimuli by caries= dentin formed with irregular structure (ranging from irregular dentinal tubules to disorganized bone like mineralized tissue. 28