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DENTAL PULP

Contents
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
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The vulnerable to injury than any other pulp cells. When irritated or injured, they contribute to one or more defense functions of the pulpodentinal complex.

Pulp defense odontoblasts are more

The smear layer Tubular sclerosis Inflammation of connective tissue

the

subjacent
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 If the injury is mild and of short duration, the response may be limited to- the dentinal tubules and the dentinoblasts in the form of

sclerotic dentin.

and/or

irritation

As the severity of the irritant increases, the underlying pulp tissue responds with progressive inflammation, first in the subdentinoblastic zone and ultimately
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The smear layer:

Scaling, abrasion, attrition, caries, and cavity preparation (cutting, grinding) leave microcrystalline debris or a smear layer that extends slightly into the dentinal tubules (smear plugs), covers the dentinal surface, and is usually several microns in thickness.

This debris is mixed with saliva, water, and/or dentinal fluid Such a closure of the dentin wound reduces both sensitivity and permeability. 6 In a way this is a defense mechanism.

Tubular sclerosis:
Produced by milder or moderately irritating agents such as slowly progressing caries, mild acute injury of cavity preparation, abrasion, erosion, attrition, 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). Considered a defense mechanism of the pulpodentinal complex because its formation alters the permeability of the tubules, blocking the 7 access of irritants to the pulp.

Peritubular dentin (physiologic sclerosis)

It is calcified secretion of the dentinoblastic process. These products, 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.
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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. This type of calcification is found in the translucent zone of carious dentin and in the dentin of severe attrition, erosion, and abrasion.
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 The peritubular dentin to be more highly mineralized than the intertubular dentin. As a result of both peritubular dentin formation and intratubular calcification, the tubules become narrower and may ultimately close completely (sclerosis).

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Inflammation.
Mild and moderate injury to the dentinoblastic processes may produce tubular sclerosis and irritation dentin. But prolonged and/or severe irritation can irreversibly affect the plasma membrane and the nucleus of the dentinoblasts, thus initiating the first step toward an inflammatory response (pulpitis).

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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

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Nature of the inflammatory response

The exudative (acute) response is
the initial immediate response of the pulpal or periapical tissue to any irritant mechanical, chemical, thermal, or microbial.

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. The dominant cells in this phase are the
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The proliferative (chronic) response is a secondary or delayed

action. Its presence depends on the ability of the exudative (acute) forces to decrease the toxicity of the irritant. It is an attempt of the connective tissue components of the pulp and periapex to form new cells (fibroblasts), blood vessels (angioblasts), and fibers. Pulpal and periapical nerve fibers 14

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, where organisms are destroyed, not nurtured. 15

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. Microorganisms and chemical irritants now have easier access to the pulp. Disturbance membrane. of the pulpodentinal
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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.

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Inflammatory changes dentinoblastic zone.

in

the

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.

inflammatory leukocytic

Central zone inflammation reflects the circumferential and apical progression of irreversible total pulpitis
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IATROGENIC PULP TESTING

According to Van Hassel, intrapulpal pressure variations provide much of the pain phenomena associated with pulpitis. He suggests further that heat and cold are two distinctly different diagnostic tools because they represent two different phenomena

1. Heat stimulation Heat causes vasodilation and subsequent increases in intrapulpal pressure. If the threshold of the sensory structures is reached, pain is produced. Intrapulpal pressure rises directly and predictably as heat is applied to the tooth.
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 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.
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Cold stimulation The response to cold of a tooth with a normal or intact pulp is immediate. Since cold decreases intrapulpal pressure, pain from this source cannot be caused by increased pressure. Brannstrom attributes the pain from cold to a hydrodynamics mechanism. The contraction of the fluid results in a rapid outward flow of fluid in the dentinal tubules and the subjacent pulpal tissue. 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 may not exacerbate the painful symptoms. If the peripheral coronal A-delta receptor units are not viable, they cannot be activated by fluid movement. Instead, cold relieves the pain immediately because the vasoconstrictor effect reduces the blood volume. This in turn lowers the intrapulpal pressure to a subthreshold level for still viable C fibers. 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.

DEPTH OF CAVITY PREPARATIONS

The deeper a cavity is cut and, therefore, the closer the odontoblastic nucleus is approached, the more severe is the injury to the odontoblast. 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, and with the cutting of the odontoblastic processes, there is an increase in irritation, with a consequent increase in the rate of production of reparative dentin
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 A reduction in dentin thickness markdly increases its permeability( pashley ,1979) by increasing the diffusional surface area in dentin. It is because of the closer the dentin prep is to the pulp, the greater the number of dentinal tubules per unit surface area and increase in the diameter of each tubule.

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 When not more than 0.5 mm of dentin remain between the base of a cavity and the pulp, each decrease of 0.1 mm produces progressively more severe pulp inflammation in low-speed

preparations without coolant.

When

low-speed preparations are made with proper cooling devices, the

floor of the preparation can be brought much closer to the pulp (0.3 mm) with less danger of severe inflammatory response.

With high-speed preparations also (200,000 rpm and more), the damage is less severe, provided adequate cooling is delivered at the interface between the bur and the 26 dentin

 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- ZnPO4 is irritating sedative dressing such as ZOE should be used

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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 , the odontoblasts require a longer period to recover.
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 However, once reparative dentin formation begins in deep cavities, its rate is more rapid but the quality is poorer than that of the dentin formed under shallow cavities.

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EFFECTIVE DEPTH
The effective depth is the area of minimum thickness of sound dentin separating the pulpal tissue from the carious lesion 2mm or more, healthy reparative reaction 0.8 2mm, unhealthy reparative reation 0.3 0.8mm, pulpal destucton

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EXTENSIVENESS OF PREPARATION
The extensiveness of the preparation has an influence on the amount of heat generated. The pulp damage is roughly proportional to the amount of tooth structure removed Zach, Cohen, 1958. 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. 31

 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.
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 In three quarter crown preparation, it is preferable to use instrument rotating at high speed for gross cutting and finish. Because, with high speed instruments, the coolant can not reach the depth of preparation & vision is obstructed. The grooving part of preparation should be done with burs revolving at

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 Full crown shoulder preparations are more harmful to the pulp than are shoulderless ones, because, in the former, the preparations are much deeper into the dentin and closer to the pulp. It is more hazardous in young tooth, as it has thin dentin.
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 During full crown preparation, occationally a pinkish to brownish discoloration becomes obvious in the dentin, it is caused by pulp hemorrhage. in such case pulp recovery is questionable. If the pulp is exposed, the treatment of choice is enodontics. The operator should not wait for

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PINLEDGE PREPARATIONS
The use of high speed instruments should be avoided as the coolant is prevented from reaching the depth of the preparation. The insertion of pins introduces the hazard of dentinal fractures or unnoticed pulp exposures. Moreover, 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. The use of fast setting ZOE or carboxylate cements could reduce or prevent the inflammation in a normal pulp. To mitigate the extra irritation from the pins, the application of calcium hydroxide in the prepared holes 36 has been advocated

SPEED OF ROTATION
When dentin is cut by rotary instruments at various speeds, an odontoblastic reaction will occur; the injury varies in degree only. The greatest amount of odontoblastic damage - 50,000 rpm without coolant. The least amount of damage 150,000 to 250,000 rpm - with coolant 300-500 rpm without coolant
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 With the increase of speeds of rotation of cutting instruments, not only is greater heat generated but there is also an increase in vibrations, which affects the pulp. Searles (1967) has pointed out that mechanical vibration during high speed drilling may be responsible for protein denaturation of the odontoblasts. The denaturation causes morphologic changes leading to destruction of the

odontoblasts.

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 5000-15,000 rpm are more destructive to the human odontoblast than speeds under 3000 rpm without coolants Marsland &
Shovelton,1957

Ultra-high speeds be used for the removal of enamel and superficial dentin Finishing of the preparations be made with very low speeds.

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 Without the use of a coolant, there is no safe speed. It may be concluded from the evidence that speeds of 3000 rpm or less and 2,00,000 rpm and above with the coolant are the safest and the speeds b/w 3000 30,000 rpm, even with coolant , are most deleterious to the pulp.
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DRY CAVITY PEPARATION

Dry cavity preparation causes greater
trauma to the pulp than preparation under water spray Cooton, 1965, Hilton & Kramer, 1967. Prolonged dehydration with air causes odontoblastic displacement and pulpal oedema, a condition that cannot be reversed by moistening the dentin after cavity preparation Morrant, 1977. Pulpal temperatures above 46 C caused irreversible changes such as stasis and thrombosis in the pulp blood vessels.
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 The circulation of pulp is altered by elevation of temperature. The intrapulpal pressure is also affected bt excessive heat generation Beveridge, Brown, 1965. Initially there is a drop of intrapulpal pressure Normal values gradually return, followed by a rise in intrapulpal

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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. Uncooled carbide bur & diamond instruments produce severe damage to the pulp. Simultaneous increase of rotational speed &pressure by various types of rotary cutting instruments cause tooth 43 temperature increases Peyton, 1955

 Increased bur pressure also may cause displacement of odontoblastic nuclei into the dentinal tubules Brannstrom, 1962.

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SIZE OF WHEELS AND BURS

The size of wheels and burs that are used is significant. 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. The coolant cannot get to the tooth as readily, resulting in more severe reactions Less severe reactions are seen when smaller instruments are employed 45 Stanley, Swerdlow, 1960.

HAND INSTRUMENTS

It has been noted that damage to pulp seemed to be more severe with the use of hand instruments as compared with burs. (Massler,JOE 1959)

Heat is not generated, but Pressure

is introduced With the use of hand instruments is responsible for the
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COOLANTS
Coolants must be employed to reduce or eliminate the heat generated by the cutting procedure.

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 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

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 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

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 There is less likelihood of pulp damage when water is used as the coolant (Zach and Cohen, 1962). Furthermore, with water cooling, the rate of removal of debris is improved (Lloyd et al, 1978).
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 The temperature elevations are significantly reduced with water cooling than that of the other methods. When the speeds of 50,000 rpm & over are used, Water in the form of a jet stream must be employed . Because, the speed at which the bur revolves creates an area of turbulence, tending to deflect the

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 Water must have sufficient pressure to penetrate the area of turbulence

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 To be effective, 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. In this way, the bur and the tooth can be covered simultaneously by the coolant. The temperature of the water cooling used during cavity preparation apparently has little significant effect on the pulp.

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POLISHING OF RESTORATIONS

Polishing of restorations without taking precautions for dissipation of heat is dangerous to the pulp (Aplin et al, 1967). A significant elevation in
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 Sandpaper discs or rubber cups, run dry at high speeds, can generate sufficient heat to damage the pulp. The generated heat can also cause enamel to fracture (Brown et al,IEJ 1978).

Therefore, polishing instruments should be run intermittently at low speeds, or in conjunction with coolants in order to reduce heat generation (Christensen and Dilts, 1968). 55

TRAUMATIC OCCLUSION
Clinical observations have led to the postulation that excessive occlusal forces may cause pulp changes such as increased

pulp stones, pulpitis, and necrosis

(Natkin and Ingle, 1963; Ramfjord and Ash, 1966).

In addition, there were disruptions of the odontoblastic layer and deposition of reparative dentin on the floor of the pulp chamber and in the root canals.
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Impressions
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 52C which is an increase of 15C unles the modeling compound is rapidly chilled

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 To avoid some of these deleterious effects, the use of rubber base impression materials may be recommended. These materials produce no heat & irritation and little pressure Langeland, 1965. The hydrocolloids also employed for impressions for inlay and crown and bridge preparations. With These materials pressure is not employed & the heat is not as

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The effect of tooth movement

Pulp injury may occur following rapid tooth movement. When a tooth is moved quickly by seperating instruments, hemorrhage is produced in the periodontal ligament. The ensuing pulp inflammation is assoisiated with edema, and the tooth may become extremely sensitive.

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 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 alterations are more severe in teeth with completed apices. The changes are proportionately more severe with increasingly greater forces.

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 There is increased deposition of reperative dentin in both the coronal and radicular portions of the pulp. Therefore the canals are extremely narrowed. Orthodontic tooth movement may also be responsible for excessive resorption of apical cementum and dentin of the tooth. In most cases the damage to the

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PHYSICAL TRAUMA
BLOWS: blow ( with or without fracture ) hemmorhage nutritional disturbances hyalinization of the pulp excessive mineralization tooth discoloration Arwill,

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 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, greater the incidence of pulp necrosis. Teeth with incomplete root formation, the chances for pulp

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 In favorable cases the color of tooth may return to normal. In general, the odontoblasts react by elaborating huge quantities of reparative dentin, mostly atubular dentin. In some teeth, the hard tissue formed is similar to bone or cementum. Such teeth may develop periapical

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FRACTURES When the pulp is not exposed, the chances for pulpal survival increase Ellis, 1970. Root fracture: 4 possible reactions to IARF s; a)Healing with calcification of pulp b)Healing with interposition of connective tissue b/w the fragments

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c) Healing with interposition of bone & connective d) Persistence of granulation tissue b/w the fragments.( most common ) Anderson, 1967. Pulp vitality is afftected by the extent of apical maturation, the location of the fracture site, and the skill of the operator in treating traumatic injuries, with early stabilization.

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 The more apical the fracture the more favorable the prognosis Zachrison, 1975. When the entire fracture is with in the alveolus, above the epithelial attachment, the chances for pulpal recovery are enhanced. When the fracture site is close to the gingival crevice, the prognosis is poorer.

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 Root fractures in young permanent teeth have high potential for healing(75-80%) and pulp vitality may be maintained without additional therapy. Healing is enhanced when there is no fragment dislocation & there is early fracture fixation. Anderson, 1981.
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CHEMICAL IRRITANTS TO THE PULP

DENTIN STERILIZING AGENTS used to destroy bacteria in the dentinal tubules in deep carious lesions. 1. Phenol it increased, rather than decreasing the permeability of dentinal tubules, therefore greater pulpal damage. (Martin, 1951)
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2. 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. Camphorated parachlorophenol and penicillin- combination of both is an effective in deep cavities but cause pulpal inflammation.
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4. Eugenol when mixed loosely with zinc oxide inhibits the action potential in the nerve fibers thus reducing pain associated with pulpal inflammation (anodyne effect). (Trowbridge et al,JOE 1982) - When placed on exposed pulp, a marked inflammatory reaction is seen. - The presence of an intervening layer of dentin is necessary to prevent an inflammatory response. 71

SILICATE CEMENT Severe pulp irritant It causes centrifugal flow of fluid in the dentinal tubules Johnson & Brannstrom, 1967 It will lead to displacement of odontoblasts. The deleterious effects of silicates on pulp are progressive Spangberg, 1973. They continuously produce irritation because they do not crystallize but
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 The pH at the time of insertion is about 2.0 and remains below 7 even after a month. ZOE or CaOH2 liner has to be used under silicates to protect the pulp

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ZINC PHOSPHATE CEMENT Pulp response is moderate. Three minutes after mixing the pH is about 3.0 It approaches neutrality in 24 to 48 hours.

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 It can cause severe pulpal damage because of its inherent irritating properties brannstrom & Nyborg, 1960. 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

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 When thin mixes are employed, ph values of 1.5-1.6 have been recordeed There is a delay in crystallization, which prolongs the irritating effects, and greater heat is generated. The pulp may be affected bye the components of the material, the heat that is liberated in setting, and the marginal leakage.

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 Thickness of dentine as great as 1.5mm can be penetrated by the acid. Thus very thin mixes should be avoided as they are more acidic. ZINC OXIDE EUGENOL CEMENT The pH is 6.6 to 8.0, thus they are the least irritating of all the cements. Causes Little pulp irritation because of eugenol .
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 ZOE should not be used to deep cavities without intervening liner Brannstrom The greater the amount of free eugenol in the mixture, the greater the chance of pulpal irritation. It provides better marginal seal than ZnPO4 cement, although leakage increases with time Norman et al, 1963.

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 It acts as effective insulating medium and prevents galvanic action of the amalgam, thus inhibiting the corrosion. The use of ZOE cement under silicate cement is contraindicated because it may discolor the silicate cement. It is also contra indicated under composite because it prevents complete polymerization.

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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
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 The cement bonds to both dentin and enamel by chelation. Adhesion to tooth structure would reduce the marginal leakage. It has got strong anti bacterial property.

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CALCIUM HYDROXIDE CEMENT

Hydrolytically

calcium, salicilates water. Alkaline in nature with pH of 9.2 to 11.7. This high alkalinity is responsible for the reparative dentin formation by releasing the large amounts of calcium released at high alkalinity . Thus it promotes the sterilization and

unstable, releasing hydroxide ions and when in contact with

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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, 1978. Etching apparently increases pulp inflammation because it removes the debris that accumulates over the dentinal 83 tubules when they are cut.

 The use of Ca(OH)2 bases or liners before acid pretreatment of enamel is highly recommended.

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COMPOSITES -Adequately cured composites are relatively biocompatible - Inadequately curing results in leaching out of components that induce long term pulpal inflammation (Phillips,11th edition)
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 Pulpal reaction is mild Heys, 1977. To reduce the irritational effects of composites, the cavity should be lined with Ca(OH)2 and covered with Zn PO4 cement prior to insertion of composite.

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GOLD FOIL the insertion of gold foil irritates the pulp Thomas , 1969. The mechanical malleting of the dentin is the offending factor. Once the foil is inserted & the malleting is stopped, the irritant is removed. If the duration of the application of malleting is short, there is a reasonable chance for pulp recovery.
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 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.

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AMALGAM Amalgam shows a minor inflammatory pulpal reaction Moller & Granath, 1973. 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.

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 The dentin discoloration results from galvanic action from the amalgam, causing the transmission of mercury ions through the dentinal tubules. The quantity of mercury ions reaching the pulp is insignificant Frikholm, 1957. The use of insulating base completely prevents the penetration.
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EFFECT OF RADIANT IRRITATIONS

X- IRRADIATION In the pulps of irradiated teeth during the formative stage - Odontoblasts are injured - Pulp cells become necrotic - Osteodentin is formed In pulps of fully formed teeth, relative to dosage, the odontoblasts appear to be extremely radioresistant (Kineldorf et al, 91 1963)

 LASER BEAM Laser damage to pulp varies with intensity of the energy. - 20 joules of energy produced mild inflammatory response in a period of 3 days 40 joules of energy produced degenerative changes in the cells, fibers and ground substance of the pulp.

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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

Pagets diseasePulp obliteration with calcification seen. mosaic pattern and dystrophic

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Rickets

Pulp horns seen extending to DEJ. delay in apical maturation enlarged pulp chamber, wide root canals. presence of draining sinus and swellings

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 Taurodontism:abnormally large pulp chambers Dens in Dente( dens invaginatus):increased risk of bacterial induced necrosis Dens evaginatus;pulp exposure is more common

pulp

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 Dentonogenesis imperfecta:pulp obliteration is seen( difficult to locate the canals)

Amelogenesis imperfecta:increased pulpal calcification

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Haemoglobinopathies
Sickle cell anemia:localized impairment of pulpal vasculature associated with asymptomatic pulpal necrosis.

Thalassemia:anesthesia of mental nerve and pulpal necrosis.

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Endocrine disorders
Diabetes:presence of angiopathies with amorphous calcification is observed. Glucocorticoids;effect connective tissue of the pulp( narrowing and obliteration of the pulp)

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Cancer
Leukemic cells of acute lymphoblastic and acute myelogenous leukemia are seen.

Other malignant cells are not detected.

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Thyroid Deficiency.
There was rapid deposition of dentin, which narrowed the lumen of the pulp, and all tissues showed a decreased amount of cellular elements.

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VITAMIN DEFICIENCY
Deficiency of certain vitamins, notably vitamin C affects fibroblasts generally and specifically affects the fibroblasts in the dental pulp.

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REACTION TO CARIOUS LESION

The initial ports of entry to the pulp for

bacteria, bacterial antigens, toxic, and allergenic components are the dentinal tubules. shows the presence of chronic inflammatory exudate, including lymphocytes, macrophages, and plasma cells.
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The pulp subjacent to deep caries lesions

Formation of tertiary dentin usually

CARIES
Dental caries is a localized, progressive decay of the teeth. It is an infectious, transmissible disease Fitzgerald, 1973. The pulp protects itself adequately in several ways, depending on the type of caries ( active or arrested) and its penetration, the structure of the tooth, and the age of the patient Massler, 1967.

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 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.
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 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 .
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 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.

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IMMUNOLOGIC REACTIONS TO CARIES In addition to the dentinal changes, the pulp apparently manufactures antibodies against the antigenic components of dental caries. These immunoglobulins are capable of migrating into the dentin. Immunoglobulins IgG, IgM, IgA, complement components C3, and C4

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ANACHORESIS
this is a process in which microorganisms carried by the bloodstream from another source localize on inflammed tissue.

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DENTINAL FLUID
Fluid flow from the dental pulp through the dentin and enamel has been demonstrated in vivo ( Bergman, 1966 ). Larger protein molecules in the fluid are apparently unable to penetrate the DEJ. The dentinal fluid is a capillary transudate from the pulp Haldi & Wynn, 1963.

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 Tooth ( dogs ) contains the same protein fractions as the blood plasma. Glucose, potassium, sodium, chlorine, magnesium, urea and alkaline phosphatase are similar in the dentinal fluid and the blood plasma Haldi, 1965.
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 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, 1965.

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CONCLUSION

THE PULP TO THE TOOTH IS LIKE THE HEART TO THE BODY

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