• Introduction • History • Definition • Development • Anatomy of pulp • Structural histology • Structural composition of pulp
•Pulpal vasculature •Functions of pulp •Regressive changes / Age changes •Pulp in clinical scenario •Pulp in systemic disorder •Conclusion •Reference
The vulnerable to injury than any other pulp cells.
Pulp defense odontoblasts are more
The smear layer Tubular sclerosis Inflammation of connective tissue
. they contribute to one or more defense functions of the pulpodentinal complex. When irritated or injured.
• As the severity of the irritant increases. the underlying pulp tissue responds with progressive inflammation. the response may be limited to. first in the subdentinoblastic zone and ultimately
.the dentinal tubules and the dentinoblasts in the form of
sclerotic dentin.• If the injury is mild and of short duration.
water.The smear layer:
• Scaling. caries. grinding) leave microcrystalline debris or a smear layer that extends slightly into the dentinal tubules (smear plugs). 6 In a way this is a defense mechanism. and cavity preparation (cutting. covers the dentinal surface. abrasion. and/or dentinal fluid • Such a closure of the dentin wound reduces both sensitivity and permeability. attrition. and is usually several microns in thickness.
• This debris is mixed with saliva.
and age changes. • It is the cumulative effect of several factors: continuing peritubular dentin formation by the dentinoblastic processes (physiologic sclerosis) and intratubular calcification (pathologic sclerosis). abrasion. attrition.Tubular sclerosis:
• Produced by milder or moderately irritating agents such as slowly progressing caries. erosion.
. • Considered a defense mechanism of the pulpodentinal complex because its formation alters the permeability of the tubules. mild acute injury of cavity preparation. blocking the 7 access of irritants to the pulp.
Peritubular dentin (physiologic sclerosis)
• It is calcified secretion of the dentinoblastic process.
. formed in the endoplasmic reticulum of the dentinoblast cell body. pass through the Golgi complex and now appear in the vesicles of the dentinoblastic process to be released as peritubular dentin matrix. • These products.
• This type of calcification is found in the translucent zone of carious dentin and in the dentin of severe attrition. and abrasion. erosion.
.Intratubular calcification (pathologic sclerosis)
• It is a physicochemical process caused by the precipitation of mineral salts within the dentinal tubules and is therefore fundamentally different from peritubular dentin.
. the tubules become narrower and may ultimately close completely (sclerosis). • As a result of both peritubular dentin formation and intratubular calcification.• The peritubular dentin to be more highly mineralized than the intertubular dentin.
• Mild and moderate injury to the dentinoblastic processes may produce tubular sclerosis and irritation dentin. thus initiating the first step toward an inflammatory response (pulpitis).
.Inflammation. • But prolonged and/or severe irritation can irreversibly affect the plasma membrane and the nucleus of the dentinoblasts.
Five facets of inflammation
• Nature of the inflammatory response • Role of the dentinoblast • Primary factors that initiate the inflammatory response • Types of inflammation • Immunologic considerations
• The dominant cells in this phase are the
• This emergency action to overcome and neutralize the injurious agent is characterized by an inflammatory edema to dilute and detoxify and by the infiltration of cells to ingest and immobilize the irritant. thermal.Nature of the inflammatory response
• The exudative (acute) response is
the initial immediate response of the pulpal or periapical tissue to any irritant mechanical. or microbial.
blood vessels (angioblasts). Its presence depends on the ability of the exudative (acute) forces to decrease the toxicity of the irritant.The proliferative (chronic) response is a secondary or delayed
action. Pulpal and periapical nerve fibers 14
. It is an attempt of the connective tissue components of the pulp and periapex to form new cells (fibroblasts). and fibers.
Sprouting of these nerve fibers occurs in pulpal areas subjacent to the injury site but also in corresponding periapical before apical progression of pathosis These elements constitute granulation tissue whose function is to repair and replace the damaged tissue Granulomatous tissue is therefore not only a healing tissue. but a defense tissue as well. 15
. not nurtured. where organisms are destroyed.
Role of the dentinoblast
The following sequence of changes can be observed as the dentinoblastic injury increases progressively: Increased permeability of the dentinal tubule because of the destructive effect of the injury to the dentinoblast and its process. Disturbance membrane. Microorganisms and chemical irritants now have easier access to the pulp. of the pulpodentinal
Aspiration of many of the dentinoblastic nuclei into the dentinal tubules (also referred to as displacement or migration).
. Irreversible dentinoblastic injury. which results in the release of the tissue injury factors.
Inflammatory changes dentinoblastic zone.
These include • dilation of capillaries and the resultant stasis of their blood flow. Autolysis can also occur if oxygen and metabolites are denied because of congestion of nearby blood vessels (within 2 to 4 minutes). The subsequent effect of such severe injuries is the further disruption of the palisade arrangement of the cells and the 18 accumulation of edematous fluid within
• Subdentinoblastic changes vasodilation. infiltration. edema.
• Central zone inflammation reflects the circumferential and apical progression of irreversible total pulpitis
He suggests further that heat and cold are two distinctly different diagnostic tools because they represent two different phenomena •
1.IATROGENIC PULP TESTING
• According to Van Hassel. pain is produced. intrapulpal pressure variations provide much of the pain phenomena associated with pulpitis. If the threshold of the sensory structures is reached. Heat stimulation • Heat causes vasodilation and subsequent increases in intrapulpal pressure.
. Intrapulpal pressure rises directly and predictably as heat is applied to the tooth.
• In an intact pulp a specific pulpal temperature must be reached before there is pain from heat.
. Therefore application of heat to normal teeth gives a delayed response. • In a tooth with an inflamed pulp an increased intrapulpal pressure already exists. therefore one would expect an immediate painful response to gradual or sudden heat increase.
The contraction of the fluid results in a rapid outward flow of fluid in the dentinal tubules and the subjacent pulpal tissue.Cold stimulation The response to cold of a tooth with a normal or intact pulp is immediate. Brannstrom attributes the pain from cold to a hydrodynamics mechanism. Since cold decreases intrapulpal pressure.
. pain from this source cannot be caused by increased pressure. Such a movement deforms intratubular and peripheral (A-delta) nerve membranes. which 22 activates an action potential.
• In advanced acute pulpitis (advanced acute pulpalgia) when coronal necrosis is present in varying degrees. cold relieves the pain immediately because the vasoconstrictor effect reduces the blood volume.
. they cannot be activated by fluid movement. • Instead. cold may not exacerbate the painful symptoms. • This in turn lowers the intrapulpal pressure to a subthreshold level for still viable C fibers. • If the peripheral coronal A-delta receptor units are not viable. • Removal of the cold results in the return to pain within 30 to 60 seconds as the intrapulpal pressure 23 returns to its former suprathreshold level.
there is an increase in irritation. therefore. and with the cutting of the odontoblastic processes. with a consequent increase in the rate of production of reparative dentin
. the closer the odontoblastic nucleus is approached. • A superficial cavity preparation that cuts the odontoblastic processes close to the dentino enamel junction usually produces only mild irritation • As the cavity depth is increased.DEPTH OF CAVITY PREPARATIONS
• The deeper a cavity is cut and. the more severe is the injury to the odontoblast.
• It is because of the closer the dentin prep is to the pulp.• A reduction in dentin thickness markdly increases its permeability( pashley .1979) by increasing the diffusional surface area in dentin.
. the greater the number of dentinal tubules per unit surface area and increase in the diameter of each tubule.
1 mm produces progressively more severe pulp inflammation in low-speed
preparations without coolant. the damage is less severe.• When not more than 0.5 mm of dentin remain between the base of a cavity and the pulp.
• With high-speed preparations also (200. each decrease of 0.
low-speed preparations are made with proper cooling devices. the
floor of the preparation can be brought much closer to the pulp (0.000 rpm and more).3 mm) with less danger of severe inflammatory response. provided adequate cooling is delivered at the interface between the bur and the 26 dentin
ZnPO4 is irritating sedative dressing such as ZOE should be used
.• The effects of further operative procedures on the pulp are influenced by the depth of the cavity prep ex: medium size cavity.ZnPO4 is acceptable deep cavity.
the odontoblasts require a longer period to recover.Depth of preparation Vs reparative dentin formation
• The speed of reparative dentin formation after cavity preparation depends on variation in cavity depts • Formation of reparative dentin begins earlier in shallow cavities & later in deep cavities • In deep cavities .
• However. its rate is more rapid but the quality is poorer than that of the dentin formed under shallow cavities. once reparative dentin formation begins in deep cavities.
unhealthy reparative reation 0. healthy reparative reaction 0.8 – 2mm.3 – 0. pulpal destucton
• The effective depth is the area of minimum thickness of sound dentin separating the pulpal tissue from the carious lesion 2mm or more.8mm.
The pulp damage is roughly proportional to the amount of tooth structure removed – Zach. 1958. 31
. Class 1 and Class 5 cavity preparations produced a much lower heat reaction than did mesioocclusodistal (MOD) or full crown preparations – Schuchard and Watkins. 1961. Cohen.EXTENSIVENESS OF PREPARATION
The extensiveness of the preparation has an influence on the amount of heat generated.
• In class – I preparations with high speeds.
. it is not desirable to sink a bur directly into a tooth fissure. because the coolant will not be able to reach the cutting area and extensive injury to the pulp will result • It is best to increase the width and the depth of fissure gradually by shallow. angular cuts.
it is preferable to use instrument rotating at high speed for gross cutting and finish. • The grooving part of preparation should be done with burs revolving at
.• In three quarter crown preparation. with high speed instruments. the coolant can not reach the depth of preparation & vision is obstructed. • Because.
• It is more hazardous in young tooth. because. in the former.• Full crown shoulder preparations are more harmful to the pulp than are shoulderless ones. the preparations are much deeper into the dentin and closer to the pulp. as it has thin dentin.
the treatment of choice is enodontics. occationally a pinkish to brownish discoloration becomes obvious in the dentin. • If the pulp is exposed.• During full crown preparation. • The operator should not wait for
. it is caused by pulp hemorrhage. • in such case pulp recovery is questionable.
The insertion of pins introduces the hazard of dentinal fractures or unnoticed pulp exposures. the deep insertion of the pin can increase pulpal irritation of an already chronically inflamed pulp The cementation of pins with ZnPO4 cement causes irritation to the pulp. Moreover. The use of fast setting ZOE or carboxylate cements could reduce or prevent the inflammation in a normal pulp.PINLEDGE PREPARATIONS
The use of high speed instruments should be avoided as the coolant is prevented from reaching the depth of the preparation. • To mitigate the extra irritation from the pins. the application of calcium hydroxide in the prepared holes 36 has been advocated
• The least amount of damage – 150. the injury varies in degree only. • The greatest amount of odontoblastic damage .with coolant 300-500 rpm – without coolant
.000 to 250.50.000 rpm .SPEED OF ROTATION
• When dentin is cut by rotary instruments at various speeds. an odontoblastic reaction will occur.000 rpm – without coolant.
• With the increase of speeds of rotation of cutting instruments. not only is greater heat generated but there is also an increase in vibrations.
. • Searles (1967) has pointed out that mechanical vibration during high speed drilling may be responsible for protein denaturation of the odontoblasts. which affects the pulp. • The denaturation causes morphologic changes leading to destruction of the
000 rpm are more destructive to the human odontoblast than speeds under 3000 rpm without coolants – Marsland &
• Ultra-high speeds be used for the removal of enamel and superficial dentin • Finishing of the preparations be made with very low speeds.
• It may be concluded from the evidence that speeds of 3000 rpm or less and 2.00. there is no safe speed. even with coolant .000 rpm.000 rpm and above with the coolant are the safest and the speeds b/w 3000 – 30. are most deleterious to the pulp.
.• Without the use of a coolant.
1977. Prolonged dehydration with air causes odontoblastic displacement and pulpal oedema.
. 1965. Hilton & Kramer. Pulpal temperatures above 46° C caused irreversible changes such as stasis and thrombosis in the pulp blood vessels.DRY CAVITY PEPARATION
Dry cavity preparation causes greater
trauma to the pulp than preparation under water spray – Cooton. a condition that cannot be reversed by moistening the dentin after cavity preparation – Morrant. 1967.
followed by a rise in intrapulpal
. • Initially there is a drop of intrapulpal pressure • Normal values gradually return.• The circulation of pulp is altered by elevation of temperature. Brown. 1965. • The intrapulpal pressure is also affected bt excessive heat generation – Beveridge.
• Simultaneous increase of rotational speed &pressure by various types of rotary cutting instruments cause tooth 43 temperature increases – Peyton. 1955
. • Uncooled carbide bur & diamond instruments produce severe damage to the pulp.NATURE OF CUTTING INSTRUMENT
• Thermal damage was greater with steel burs than with carbide burs Marsland and Shoelton (1957) and Weiss et al (1963) • With proper cooling. carbide burs produce negligible pulp damage.
. 1962.• Increased bur pressure also may cause displacement of odontoblastic nuclei into the dentinal tubules – Brannstrom.
. • The larger sizes produce greater pulp damage. owing to increased heat generation and the peripheral speed of larger disc is significantly higher than that of a small disk at the same rpm. Swerdlow. resulting in more severe reactions • Less severe reactions are seen when smaller instruments are employed – 45 Stanley. • The coolant cannot get to the tooth as readily.SIZE OF WHEELS AND BURS
• The size of wheels and burs that are used is significant.
• It has been noted that damage to pulp seemed to be more severe with the use of hand instruments as compared with burs.JOE 1959)
Heat is not generated. but Pressure
is introduced With the use of hand instruments is responsible for the
• Coolants must be employed to reduce or eliminate the heat generated by the cutting procedure.
• The coolants in use are: a)Air spray b)A combination of water and air,as a water spray c)Water applied through a hollow bur d)Water as a jet stream
• Air blasts are damaging to the pulp. • A blast of air on the dentin, with either an ordinary chip syringe or compressed air, for 10 sec is enough to produce displacement of odontoblastic nuclei – Langeland, 1972. • Therefore cavity cutting should not be performed with air cooling alone. • During cavity toilet, the cavity should not be dried with air blasts ;cotton
• There is less likelihood of pulp damage when water is used as the coolant (Zach and Cohen.
. Furthermore. the rate of removal of debris is improved (Lloyd et al. 1962). 1978). with water cooling.
• When the speeds of 50. the speed at which the bur revolves creates an area of turbulence.000 rpm & over are used. • Because. Water in the form of a jet stream must be employed .• The temperature elevations are significantly reduced with water cooling than that of the other methods. tending to deflect the
• Water must have sufficient pressure to penetrate the area of turbulence
the bur and the tooth can be covered simultaneously by the coolant. the water should be delivered directly at the point of contact between the bur and the tooth • High-speed cutting should be done with a brush stroke similar to that employed by a painter using water colors. • The temperature of the water cooling used during cavity preparation apparently has little significant effect on the pulp. In this way.• To be effective.
1967).POLISHING OF RESTORATIONS
• Polishing of restorations without taking precautions for dissipation of heat is dangerous to the pulp (Aplin et al. • A significant elevation in
. can generate sufficient heat to damage the pulp. • The generated heat can also cause enamel to fracture (Brown et al. or in conjunction with coolants in order to reduce heat generation (Christensen and Dilts.
• Therefore. run dry at high speeds.IEJ 1978). polishing instruments should be run intermittently at low speeds.• Sandpaper discs or rubber cups. 1968).
In addition. pulpitis. Ramfjord and Ash. 1966).
. 1963. there were disruptions of the odontoblastic layer and deposition of reparative dentin on the floor of the pulp chamber and in the root canals.TRAUMATIC OCCLUSION
• Clinical observations have led to the postulation that excessive occlusal forces may cause pulp changes such as increased
pulp stones. and necrosis
(Natkin and Ingle.
• Temperatures inside the pulp chamber can be significantly increased when impressions are taken with modeling compound that has been heated in open flame. Intrapulpal temperature remains high for more than 3 min rising to ana average of 52˚C which is an increase of 15˚C unles the modeling compound is rapidly chilled –
• To avoid some of these deleterious effects. • With These materials pressure is not employed & the heat is not as
. 1965. • These materials produce no heat & irritation and little pressure – Langeland. • The hydrocolloids also employed for impressions for inlay and crown and bridge preparations. the use of rubber base impression materials may be recommended.
. • The ensuing pulp inflammation is assoisiated with edema. and the tooth may become extremely sensitive. hemorrhage is produced in the periodontal ligament. • When a tooth is moved quickly by seperating instruments.The effect of tooth movement
• Pulp injury may occur following rapid tooth movement.
• The forces involved in orthodontic tooth movement create disturbances in the circulation of the pulp resulting in reduction of the supply of nutrients to the odontoblasts. • The changes are proportionately more severe with increasingly greater forces.
. • The alterations are more severe in teeth with completed apices.
• Orthodontic tooth movement may also be responsible for excessive resorption of apical cementum and dentin of the tooth.• There is increased deposition of reperative dentin in both the coronal and radicular portions of the pulp. • Therefore the canals are extremely narrowed. • In most cases the damage to the
BLOWS: blow ( with or without fracture ) hemmorhage nutritional disturbances hyalinization of the pulp excessive mineralization tooth discoloration Arwill.
greater the incidence of pulp necrosis. the chances for pulp
.• It is impossible to predict the extent of damage to the pulp. • The pulpal reaction depends on the severity of the hemorrhage & completion of the root. • The greater the trauma of tooth. • Teeth with incomplete root formation.
• In general. the hard tissue formed is similar to bone or cementum. mostly atubular dentin.• In favorable cases the color of tooth may return to normal. the odontoblasts react by elaborating huge quantities of reparative dentin. • In some teeth. • Such teeth may develop periapical
Root fracture: • 4 possible reactions to IARF s.FRACTURES • When the pulp is not exposed. 1970. the chances for pulpal survival increase – Ellis. a)Healing with calcification of pulp b)Healing with interposition of connective tissue b/w the fragments
and the skill of the operator in treating traumatic injuries.
. • Pulp vitality is afftected by the extent of apical maturation.( most common ) Anderson.c) Healing with interposition of bone & connective d) Persistence of granulation tissue b/w the fragments. 1967. the location of the fracture site. with early stabilization.
the prognosis is poorer. • When the fracture site is close to the gingival crevice.
. • When the entire fracture is with in the alveolus. the chances for pulpal recovery are enhanced. above the epithelial attachment.• The more apical the fracture the more favorable the prognosis – Zachrison. 1975.
.• Root fractures in young permanent teeth have high potential for healing(75-80%) and pulp vitality may be maintained without additional therapy. 1981. • Healing is enhanced when there is no fragment dislocation & there is early fracture fixation.
Phenol – it increased. rather than decreasing the permeability of dentinal tubules. 1951)
. therefore greater pulpal damage. (Martin.CHEMICAL IRRITANTS TO THE PULP
• DENTIN STERILIZING AGENTS – used to destroy bacteria in the dentinal tubules in deep carious lesions. 1.
Silver nitrate – silver salts diffuse rapidly through the dentinal tubules and regardless of the depth of the cavity eventually reach the pulp tissue resulting in an inflammatory reaction.
3.2.combination of both is an effective in deep cavities but cause pulpal inflammation. Camphorated parachlorophenol and penicillin.
.4.The presence of an intervening layer of dentin is necessary to prevent an inflammatory response.JOE 1982) . .When placed on exposed pulp. (Trowbridge et al. a marked inflammatory reaction is seen. Eugenol – when mixed loosely with zinc oxide inhibits the action potential in the nerve fibers thus reducing pain associated with pulpal inflammation (anodyne effect).
1973. The deleterious effects of silicates on pulp are progressive – Spangberg. 1967 It will lead to displacement of odontoblasts.SILICATE CEMENT Severe pulp irritant It causes centrifugal flow of fluid in the dentinal tubules – Johnson & Brannstrom. They continuously produce irritation because they do not crystallize but
0 and remains below 7 even after a month. • ZOE or CaOH2 liner has to be used under silicates to protect the pulp
.• The pH at the time of insertion is about 2.
Three minutes after mixing the pH is about 3.
.0 It approaches neutrality in 24 to 48 hours.ZINC PHOSPHATE CEMENT Pulp response is moderate.
1960.• It can cause severe pulpal damage because of its inherent irritating properties – brannstrom & Nyborg. • toxicity is more pronounced when it is placed in deep cavities. • In deep cavities it should not be used without an intervening liner of Ca(OH)2 • Thick mixes should be used to
and the marginal leakage.5-1.• When thin mixes are employed. ph values of 1. and greater heat is generated. which prolongs the irritating effects.6 have been recordeed • There is a delay in crystallization. • The pulp may be affected bye the components of the material.
. the heat that is liberated in setting.
6 to 8. thus they are the least irritating of all the cements.5mm can be penetrated by the acid.0.
. ZINC OXIDE EUGENOL CEMENT The pH is 6.• Thickness of dentine as great as 1. Causes Little pulp irritation because of eugenol . • Thus very thin mixes should be avoided as they are more acidic.
the greater the chance of pulpal irritation.
. although leakage increases with time – Norman et al. 1963.• ZOE should not be used to deep cavities without intervening liner – Brannstrom • The greater the amount of free eugenol in the mixture. • It provides better marginal seal than ZnPO4 cement.
. thus inhibiting the corrosion. • It is also contra indicated under composite because it prevents complete polymerization. • The use of ZOE cement under silicate cement is contraindicated because it may discolor the silicate cement.• It acts as effective insulating medium and prevents galvanic action of the amalgam.
GLASS IONOMER CEMENT Pulpal response is mild. Pulpal reaction is greater than ZOE – plant. 1971 and less than ZnPO4 cement ZINC POLYCARBOXYLATE CEMENT Pulpal response is mild The pH of set cement is 5.0 to 6.0 Penetration of polyacrylic acid into the dentinal tubules is less because
. • It has got strong anti bacterial property. • Adhesion to tooth structure would reduce the marginal leakage.• The cement bonds to both dentin and enamel by chelation.
7. Alkaline in nature with pH of 9.CALCIUM HYDROXIDE CEMENT
calcium. releasing hydroxide ions and when in contact with
. salicilates water.2 to 11. Thus it promotes the sterilization and
unstable. This high alkalinity is responsible for the reparative dentin formation by releasing the large amounts of calcium released at high alkalinity .
1978. • Etching apparently increases pulp inflammation because it removes the debris that accumulates over the dentinal 83 tubules when they are cut.
.ACID ETCHING -It does not cause any irreversible damage to the pulp -It only causes early inflammatory reaction which subsides (Nakabayashi-hybridisation of dental tissues) • Pulp reaction to acid etchants have been rated as mild to moderate – macko et al.
• The use of Ca(OH)2 bases or liners before acid pretreatment of enamel is highly recommended.
.COMPOSITES -Adequately cured composites are relatively biocompatible .Inadequately curing results in leaching out of components that induce long term pulpal inflammation (Phillip’s.
1977. • To reduce the irritational effects of composites.• Pulpal reaction is mild – Heys.
. the cavity should be lined with Ca(OH)2 and covered with Zn PO4 cement prior to insertion of composite.
there is a reasonable chance for pulp recovery. the irritant is removed. • Once the foil is inserted & the malleting is stopped. 1969.
. • If the duration of the application of malleting is short. • The mechanical malleting of the dentin is the offending factor.GOLD FOIL • the insertion of gold foil irritates the pulp – Thomas .
.• The use of gold foil should be avoided in the teeth of youngesters because pulps are larger dentinal tubules are wider & dentin thickness is less.
AMALGAM • Amalgam shows a minor inflammatory pulpal reaction – Moller & Granath. • Liners are necessary in order to prevent discomfort due to the thermal conductivity of the metal – Dachi & Stigers. 1967 and to help reduce the effects of the pressure of amalgam condensation.
• The quantity of mercury ions reaching the pulp is insignificant – Frikholm. 1957.
.• The dentin discoloration results from galvanic action from the amalgam. • The use of insulating base completely prevents the penetration. causing the transmission of mercury ions through the dentinal tubules.
Osteodentin is formed In pulps of fully formed teeth.Pulp cells become necrotic . the odontoblasts appear to be extremely radioresistant (Kineldorf et al.Odontoblasts are injured .EFFECT OF RADIANT IRRITATIONS
• X.IRRADIATION In the pulps of irradiated teeth during the formative stage . relative to dosage. 91 1963)
fibers and ground substance of the pulp.20 joules of energy produced mild inflammatory response in a period of 3 days 40 joules of energy produced degenerative changes in the cells.
.• LASER BEAM Laser damage to pulp varies with intensity of the energy. .
Pulp in systemic disorders
In viral infection:• Herpes virus: HSV I : May include multiple unilateral necrotic pulp Herpes zoster: effect the peripheral nerve ending in the pulp .pulp necrosis
Paget’s diseasePulp obliteration with calcification seen. mosaic pattern and dystrophic
• • • Pulp horns seen extending to DEJ. wide root canals. delay in apical maturation enlarged pulp chamber. presence of draining sinus and swellings
pulp exposure is more common
.• Taurodontism:abnormally large pulp chambers • Dens in Dente( dens invaginatus):increased risk of bacterial induced necrosis • Dens evaginatus.
• Dentonogenesis imperfecta:pulp obliteration is seen( difficult to locate the canals)
• Amelogenesis imperfecta:increased pulpal calcification
• Thalassemia:anesthesia of mental nerve and pulpal necrosis.
• Sickle cell anemia:localized impairment of pulpal vasculature associated with asymptomatic pulpal necrosis.
• Glucocorticoids.effect connective tissue of the pulp( narrowing and obliteration of the pulp)
• Diabetes:presence of angiopathies with amorphous calcification is observed.
• Other malignant cells are not detected.
• Leukemic cells of acute lymphoblastic and acute myelogenous leukemia are seen.
which narrowed the lumen of the pulp. and all tissues showed a decreased amount of cellular elements.
• There was rapid deposition of dentin.
• Deficiency of certain vitamins.
. notably vitamin C affects fibroblasts generally and specifically affects the fibroblasts in the dental pulp.
and plasma cells.REACTION TO CARIOUS LESION
The initial ports of entry to the pulp for
The pulp subjacent to deep caries lesions
Formation of tertiary dentin usually
. bacterial antigens. and allergenic components are the dentinal tubules. macrophages. including lymphocytes. shows the presence of chronic inflammatory exudate.
• Dental caries is a localized. and the age of the patient – Massler. 1967. the structure of the tooth. depending on the type of caries ( active or arrested) and its penetration. • It is an infectious. 1973. progressive decay of the teeth. transmissible disease – Fitzgerald. • The pulp protects itself adequately in several ways.
• The pulp reacts to the process of dental caries by forming sclerotic dentin in the primary dentinal tubules and also by the elaboration of reparative dentin under the region of the involved tubuls. • Thus the pulp volume is reduced and the aging process of the pulp is accelerated.
• The formation of reparative dentin increases the collagenous portion of the pulp. • When the caries progresses more rapidly than the elaboration of reparative dentin, the blood vessels of the pulp dilate and the chronic inflammatory cells are scattered .
• As the decay comes closer to the pulp, inflammatory cells are found more scattered sub adjacent to the region of involved dentinal tubules and finally frank exposure occurs.
complement components C3. and C4
. IgM. IgA.IMMUNOLOGIC REACTIONS TO CARIES • In addition to the dentinal changes. Immunoglobulins IgG. the pulp apparently manufactures antibodies against the antigenic components of dental caries. • These immunoglobulins are capable of migrating into the dentin.
• this is a process in which microorganisms carried by the bloodstream from another source localize on inflammed tissue.
• Fluid flow from the dental pulp through the dentin and enamel has been demonstrated in vivo ( Bergman. • Larger protein molecules in the fluid are apparently unable to penetrate the DEJ. 1966 ). • The dentinal fluid is a capillary transudate from the pulp – Haldi & Wynn. 1963.
magnesium. sodium. • Glucose. urea and alkaline phosphatase are similar in the dentinal fluid and the blood plasma – Haldi.
. chlorine. potassium.• Tooth ( dog’s ) contains the same protein fractions as the blood plasma. 1965.
.• Systemically administered chemotherapeutic agents such as sulfonamides and penicillins also have been detected in the dentinal pulp fluid in the same concentration as in the blood plasma – Haldi & John.
THE PULP TO THE TOOTH IS LIKE THE HEART TO THE BODY