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Dental pulp


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  • 1. CONTENTS • INTRODUCTION • DEVELOPMENT • ANATOMY o General features o Pulps of maxillary teeth o Pulps of mandibular teeth o Coronal pulp o Radicular pulp o Apical foramen o Accessory canals • STRUCTURAL FEATURES • FUNCTIONS o Inductive o Formative o Nutritive o Protective o Defensive • VASCULAR SUPPLY • INNERVATION • CLINICAL CONSIDERATIONS • THE FUTURE • CONCLUSION • REFERENCES
  • 2. INTRODUCTION : Rapid advances in the basic sciences and the development of sophisticated instrumentation have had a profound effect on one know ledge of every organ in the body. The dental pulp is no exception. There are some technical difficulties in deriving information on the dental pulp an organ or tissue that is difficult to see because it is encased by the hardest materials in the body. “WHY MAKE SUCH A BIG ISSUE ABOUT A LITTLE TISSUE? This is because this little tissue has created a big issue. The best root filling is the healthy pulp. The pulp is a soft tissue of mesenchymal origin with specialized cells, the odontoblasts arranged peripherally in direct contact with the dentin matrix. It is enclosed by the rigid mineralized dentin and this admits its ability to increase in volume during episodes of vasodilatation and increased tissue presence. Following tooth development, pulp retains its ability to produce dentin throughout life. This enables vital pulp to partially compensate for the losses of enamel or dentin caused by mechanical trauma or disease etc. Thus, knowledge about pulp provides a firm biological basis for clinical decision making.
  • 3. DEVELOPMENT Pulp is basically derived from the cephalic neural crest. During the sixth week of embryonic life, tooth formation begins with the development of the primary epithelial bands in the upper and lower jaws. This continuous horse-shaped bands of thickened epithelium cry quickly divides into o Vestibular lamina o Dental lamina Within the dental lamina, continued and localized proliferative activity leads to the formation of series of epithelial ingrowths into the ectomesenchyme. (primitive 2 or 3 cell thick layered epithelial covering an embryonic connective tissue) at sites corresponding to future deciduous teeth. From this point, tooth development proceeds in 3 stages • Bud • Cap and • Bell Bud stage Cap stage Bell stage
  • 4. Bud stage : Is represented by the first epithelial ingrowths – or incursions into the ectomesenchyme of the jaw. Cap stage : Further proliferation into the ectomesenchyme and cellular density increases immediately adjacent to the epithelial ingrowth. This process is classically referred to as “condensation” of the ectomesenchyme. The epithelial ingrowth, which superficially resembles a “cap” sitting on a ball of condensed ectomesenchyme is called enamel or dental organ – eventually forms enamel of the tooth. The ball of condensed ectomesenchyme cells called DENTAL PAPILLA – forms dentin and pulp. DENTAL PAPILLA
  • 5. Bell stage : Continued growth leads to the enamel organ resembling a bell as the undersurface deepens. The cells within the dentin papilla undergo cytodifferentiation into a peripheral layer of odontoblasts and a central mass of fibroblasts. This change is induced by signals originating in the internal enamel epithelium. Once the odontoblasts begin to lay down dentin, the dental papilla becomes by convention, the dental pulp. Vascularization of the developing pulp also starts during this stage, with branches entering the base of the papilla. The vascularization of the odontoblast layer increases as dentin is progressively laid down. Pioneer nerve fibers approach the developing tooth during bud-cap stage but they penetrate the dental papilla after dentin begins. Here, we see the life cycle of the ameloblast related to that of the odontoblast.
  • 6. 1) The ameloblast begins to differentiate first 2) The peripheral ectomesenchymal cells divide, with some daughter cells migrating below the odontoblast layer. 3) Acting from a signal from the ameloblast, the pre-odontoblasts begins to differentiate. 4) Synthetic organelles begin to increase in size and number. 5) Cell becomes polarized, nucleus moves basally. Number of odontoblastic process begin to form and begins to secrete matrix. 6) Odontoblast retracts as matrix is being laid down, leaving behind a single main process. 7) Once the first layer of dentin is laid down, the differentiated ameloblast begins to deposit matrix. ANATOMY : General features : The dental pulp occupies the center of each tooth and shapes itself to a miniaturization of the tooth. Every person normally has a total of 52 pulp organs, 32 in the permanent teeth and 20 in deciduous dentition. The residence of the pulp is called the pulp cavity surrounded by dentin on all sides except at the apical foramen. • Total volumes of all the permanent teeth pulp organs is 0.38cc. • Mean volume of a single adult human pulp is 0.02cc. Molar pulps are 3-4 times larger than incisor pulps.
  • 7. The pulp cavity may be divided into a coronal portion – the pulp chamber and a radicular portion – the root canal. In single rooted teeth, the pulp chamber gradually merges into the root canal, but in multirooted teeth, there is a single pulp chamber and more than one root canal. There are canal orifices which are openings in the floor of the pulp chamber leading into the root canals. They are not separate structures but are continuous with both the pulp chamber and root canals. Coronal pulp : The pulp chamber has a roof, floor, mesial, buccal, lingual and distal surfaces. There are pulp horns which are acc extending of the pulp chamber directly under a cusp or developmental lobe. The number of these of these horns, thus depends on the cuspal number. Radicular pulp : Or the root canal is that portion of the pulp cavity from the canal orifice to the apical foramen. They are not always straight, and vary in size, shape and number. It may divided for convenience into the coronal, middle and apical third portions. The radicular portions of the pulp are continuous with the periapical connective tissue through the apical foramen. Apical foramen : Is an aperture at or near the apex of a root through which the blood vessels and nerves of the pulp enter or leave the pulp cavity. The anatomy of this is partially determined by the number and location of apical blood vessels present at the time of formation of the apex. The average size of the apical foramen of maxillary teeth in adults is 0.4mm, in mandibular teeth it is 0.3mm. In young, incompletely developed
  • 8. teeth the apical foramen is funnel shaped, with the wider portion extending outward. The mouth of the funnel is filled with periodontal tissue that is later replaced by dentin and cementum. As the root develops, the apical foramen becomes narrower. The inner surface of the root apex becomes lined with cementum, which may extend for a short distance into the root canal (1mm-1.5mm). Also, the apical foramen is not always the most constricted portion of the root canal. Constrictions can and do occur before the extremity of the root is reached. And the apical foramen is not always in the center of the root apex. It may exit on the mesial, distal, labial or lingual surface of the root, usually slightly eccentrically. Anatomic studies have shown that the apical foramen coincides within the anatomic apex in only 17 to 46% of the cases and it is located on an average of 0.4 to 0.7mm away from the anatomic apex. As a general rule, the root apex is completely formed about 2-3 years after eruption of the tooth. Accessory canals : Occasionally, during formation of the root sheath, a break develops in the continuity of the sheath, producing a small gap. When this occurs, dentinogenesis does not take place opposite the defect. The result is a small “accessory canal”. They can become established anywhere along the root but are found to be most numerous in the apical third. They create a periodontal-endodontic pathway of communication and a possible portal of entry in to the pulp if the periodontal tissues lose their integrity (in case of periodontal disease) Accessory foramina are also present, which are openings of the accessory and lateral canals in the root surface.
  • 9. Pulps of maxillary teeth : In the central incisor – pulp is somewhat shovel shaped with 3 pulp horns which are short lateral incisor has 2 pulp horns and the longest pulp is cuspid with an elliptical cross section buccolingually, with 1 pulp horn. First premolar has large pulp chamber occlusocervically dividing into 2 smooth funnel shaped root. The second premolar is similar but has only one root which tapers at about its midpoint. Molars : The pulp chamber of maxillary first molar is the largest in the dental arch, with 4 pulp horns – mesiobuccal, distobuccal, mesiopalatal and disto palatal. The arrangement of the pulp horns gives the pulpal root a rhomboidal shape is cross section, while the pulpal floor is triangular in cross section. There are usually 3 roots with usually 3 canals situated in, mesiobuccal, distobuccal and palatal. The mesiobuccal canal is the narrowest of the three. The palatal root canal is the largest having the largest diameter of the three. Maxillary second molars have a pulp chamber similar to the first molar except that it is narrower mesiodistally and the 3 root canals are more closely grouped. Pulps of mandibular teeth : The pulp chamber of central incisors in small and flat mesiodistally. The three distinct pulp horns present in a recently erupted tooth become calcified and disappear early in life due to constant masticatory stimulus. Mandibular lateral incisor is parallel to central incisor but only larger in dimension. The mandibular cuspid resembles the maxillary cuspid with smaller dimensions. Only one pulp horn is present in the adult tooth.
  • 10. Mandibular first premolar has a pulp chamber that is narrow mesiodistally but wider buccolingually. It has a prominent buccal pulp horn, and a small lingual pulp horn that may disappear with age. Mandibular second premolar is similar to the first premolar except that the lingual pulp horn is more prominent. The roof the mandibular first molar pulp chamber is often rectangular in shape with 4 pulp horns – mesiobuccal, distobuccal, mesiolingual and distolingual and the floor is rhomboidal in shape. Three root canals are usually present but at times a second distal canal may also be present. Mandibular second molar has a pulp chamber that is smaller than the first molar and the roots are closer together. Three root canals are usually present. Primary Pulp Organs Function for a shorter period of time than do permanent pulps. Average length of time a primary pulp functions is about 8.3 years. This amount of time can be divided into 3 time periods 1) Pulp organ growth 2) Pulp maturation 3) Pulp regression 1. When crown and roots are developing. 1 year 2. Root is completed till root resorption. 3 yrs 9 months 3. From root resorption till exfoliation. 3 years, 6 months Permanent Pulp Organs : During crown formation the pulps of primary and perm teeth are morphologically identical. It takes 5 years in permanent teeth. During this time the organs are highly cellular, exhibiting a high mitotic rate specially in
  • 11. cervical region primary teeth also never attain the same extent of neural development seen in permanent organ. STRUCTURAL ELEMENTS Dental pulp is a loose connective tissue and made up of a combination of cells embedded in an extra cellular matrix of fibers in a semifluid gel. It contains 75% by wt of water and 25% organic material. MORPHOLOGIC ZONES OF PULP :
  • 12. 1. Odontoblast layer : The outermost stratum of cells of healthy pulp is the odontoblast layer. This layer is located immediately subadjacent to the predentin, the odontoblast processes, however, pass on through the predentin, into the dentin. Consequently, the odontoblast layer is actually composed of the cell bodies of odontoblasts. Additionally, capillaries, nerve fibers and dendritic cells may be found among the odontoblasts. This layer is the “EFFECTOR SYSTEM” of the pulp; all the other elements are either supportive or protective of the cells forming dentin or programmed to replace them. In the coronal portion of a young pulp, the odontoblasts assume a tall columnar form, the tight packing together of these cells – tall and slender produces the appearance of a palisade. The odontobalsts vary in height; consequently, their nuclei are not all at the same level and are aligned in a staggered array. This often produces the appearance of a layer 3-5 cells in thickness. Between odontoblasts, there are small intercellular spaces, approximately 300-400 A0 in width. The odontoblast layer in the coronal pulp contains more cells unit area than in the radicular pulp. Because there are fewer dentinal tubules per unit area in the root than in the crown of the tooth, the odontoblast cell bodies are less crowded and are able to spread out laterally. Between adjacent odontoblasts, there are a series of specialized cell-to-cell junctions. Cell poor zone : Immediately subjacent to the odontoblast layer in the coronal pulp, there is often a narrow zone approximately 40mm in width that is relatively free of cells. It is traversed by capillaries, unmyelinated nerve fibers and the slender cytoplasmic processes of fibroblasts. The presence or absence of the
  • 13. cell poor zone depends on the functional status of the pulp. It may not be apparent in young pulps, where dentin forms rapidly, or in older pulps, where reparative dentin is being produced. Cell-rich zone : Usually conspicuous in the subodontoblastic area is a stratum consisting a relatively high proportion of fibroblasts, compared with a more central region of the pulp. It is much more prominent in the coronal pulp than in the radicular pulp. Besides fibroblasts, the cell-rich zone may include a number of macrophages, dendritic cells and lymphocytes. On the basis of evidence obtained in rats molar teeth, it has been suggested that the cell-rich zone forms as a result of peripheral migration of cells populating the central regions of the pulp commencing at about the time of tooth eruption. Although cell division within the cell-rich zone is a rare occurrence in normal pulps, death of odontoblasts causes a great increase in the rate of mitosis. Because irreversibly injured odontoblasts are replaced by cells that migrate from the cell-rich zone, onto the inner surface of dentin, this mitotic activity is probably the 1st step in formation of a new odontoblast layer. Pulp proper : This is the central mass of the pulp. It contains the larger blood vessels and nerves. The connective tissue cells in this zone consist of fibroblasts or pulpal cells.
  • 14. Supraodontoblast region : Beginning from the outside, the potential space between the odontobalst layer and the predentin could be described as the supraodontoblast layer. 2 structures are located in this region. 1. Unsheathed axons: Found almost exclusively in the crown. These have been described as the predentinal plexus of BRADLAW. They are not a true plexus (network) but an area where a number of axons congregate. It is not clear whether many axons end in this plexus. But, these axons are in an ideal position to sense changes in fluid movement then the dentinal tubules as well as changes in the extracellular fluid composition, which, because of the barrier properties of the odontoblast layer, will be delayed in reaching the core of the pulp. 2. Dendritic antigen presenting cells: They are at least 50µm long and have 3 or more main dendritic processes which branch. The dendritic cells act at least primarily, as antigen presenting cells, stimulating the division and activity of T-lymphocytes. They initiate primary immune response. The region, thus, deserves some special mention as (after the odontoblastic processes) this is the first area at which external stimuli can be detected in the pulp.
  • 15. CELLS Fibroblasts : The pulp organ is said to consist of specialized connective tissue because it lacks elastic fibers. The fibroblasts are the basic cells of the pulp and also the most numerous cell type. As their name implies, they function in collagen fiber formation throughout the pulp during the life of the tooth. They are active in collagen synthesis. The cells synthesize type I and III collagen as well as proteogycans and glycosaminoglycans. Fibroblasts of the pulp are said to be like “Peter Pan” because they never really “grow up”. These cells do seem to remain in a relatively undifferentiated modality when compared with fibroblasts of other connective tissue of the body. They have typical stellate shape and extensive processes that contact and are joined by intercellular junctions to the processes of other fibroblasts. In young pulp, the cells divide and are active in protein synthesis, but in the older pulp, they appear rounded or spindle shaped with short processes and exhibit fewer intracellular organelles. They are then termed fibrocytes. In the course of development, the relative number of cellular elements in the dental pulp decreases whereas the fibre population increases. The fibroblasts of the pulp, in addition to forming the pulp matrix, also have the capability of ingesting and degrading this same matrix. These cells thus have a dual function with pathways for both synthesis and degradation in the same cell. Due to this they are responsible for the collagen turnover in the pulp.
  • 16. Odontoblasts : Odontoblasts are the second most prominent cell in the pulp. They reside adjacent to the predentin with cell bodies in the pulp, and cell processes in the dentinal tubules. They are approx. 5-7 µm in diameter and 25-40 µm in length. Morphologic variations occur in odontoblasts, ranging from tall columnar cells in the crown to a low columnar type in the middle of the root. From an SEM study, French scientists have demonstrated that the odontoblast cell bodies appear tightly packed in the pulp horn and successively pear shaped, spindle shaped, club shaped for globular from crown to the apex. A FULLY DIFFERENTIATED ODONTOBLAST
  • 17. The odontoblast is a highly differentiated cell in the pulp. Both fibroblasts and odontoblasts are derived from the mesenchyme but odontoblasts are more highly differentiated cells than the fibroblasts. The main function of the odontoblaasts is the production of dentin. The cell body manufacturers the matrix material the material is transported to and secreted from the odontoblastic processes. Under SEM odontoblasts appear as large, closely aligned, multilayered sweet potato shaped cells. They average 3-4µm in width to 8- 10 µm in length. The ultrastructural features of the odontoblast have been subject to numerous investigations. The cell body of the active odontoblast has a large, nucleus that may contain up to 4 nucleoli. Nucleus is situated at the basal end of the cell and is contained within a nuclear envelope. A well developed golgi complex, centrally located in supranculear cytoplasm consists of an assembly of smooth walled vesicles and cisternae. Numerous mitochondria are evenly distributed throughout the cell body. Rough endoplasmic reticulum is particularly prominent, consisting of closely stacked cisternae. Odontoblastic process : Each process traverses the predentin and then occupies a canaliculus in the dentin, predominantly filling the lamina of the dentinal tubules. The odontoblastic process called dentinal fibers or tomes fibers are cytoplasmic tubular projections, usually devoid of major cytoplasmic organ cells. Processes are larger at pulpal end than at the periphery (4:1). Microtubules and microfilaments are the principal components of odontoblastic processes. Microtubules extend from the cell body out into the process. These straight structures impart the impression of rigidity.
  • 18. The plasma membrane of the odontoblastic process closely approximates the wall of the dentinal tubules. The extent to which the process extends into dentin has been a controversy. It has been long thought that the process extends to the full length of dentin (2-3mm). But ultra structural studies using TEM have described the process as being limited to the inner third of the dentin with the outer 2/3rd comprised of extracellular fluid. But other studies employing SEM, have described the processes extending further into the tubule, often as for as the DEJ. More recently, confocal microscopy using rat molars, concluded that the processes doe not extend upto the DEJ, except during the early stages of tooth development. But other studies are warranted. After the initial dentin formation, the odontoblasts, via the processes can still modify dentin structure by producing peritubular dentin. This is a hypermineralized cuff with little organic matrix in the tubule, decreasing the diameter of the tubule. The odontoblastic processes are bathed by intercellular fluid from the dental pulp. Intercellular junctions : Small regions of the plasma membranes between cells (intercellular junctions) are visible only by electron microscopy. There are 3 types of intercellular junctions. 1) Impermeable (tight junction) 2) Adhering (zonula adherence) 3) Communicating (nexuses) 1. Impermeable junctions help the cell maintain a distinct internal environment. In these junctions, the plasma membranes of
  • 19. adjacent cells appear to fuse and afford a tight seal between these cells. Found mainly in the apical part of odontoblasts in young teeth. 2. Adhering junctions are maintained by desomsomes, which are intercellular bridges seen in light microscopy. There are 3 types of desomsomes - Belt - Spot - Hemidesmosomes Spot desmosomes are located in the apical part of the odontoblastic cell bodies mechanically join odontoblasts together. They promote adhesion between cells. 3. Communicating junctions also called gap junctions, are structures that mediate direct transfer of chemical messages between cells. They enable cells to exchange nutrients and signal molecules for co-ordination of function. Numerous gap junctions provide low- resistance pathways through which electrical excitation can pass between cells. These junctions are most numerous during the formation of primary dentin gap junctions crust special proteins called connections in their plasma membrane which contain pores 15A0 in width gap junctions and desmosomes have also been observed joining odontoblasts to the processes of fibroblasts in the subodontoblastic area. Odontoblastic communications : The odontoblastic processes are in contact with adjacent processes through an extensive lateral branch system. The odontoblasts also contact cells more centrally located in the pulp through fine protoplasmic processes,
  • 20. possibly owing to the presence of fibronectin, a meditator of cell-to-cell adhesion. Thus, the odontoblasts may be regarded as part of a mesenchymal synctium. This cellular contact is significant because of an odontoblast is injured, other odontobalsts are affected. The cells on either side are affected by the breakdown products of the injured odontoblasts when the dentin is injured through operative procedures; the normal palisade arrangement of the odontobalsts is altered resulting in disruption of the continuity of these cells. Thus, injury to the dentin of the tooth creates a reaction within the pulp. DEFENCE AND OTHER CELLS : Some of the cells in the pulp are defence cells. Histiocytes or resting wandering cells are usually found near the blood vessels. They have long slender branching processes and are able to withdraw these processes and change quickly into macrophages when the need arises. Undifferentiated mesenchymal cells are present in the pulp, as they are in all connective tissue. They are capable of becoming macrophages during injury. They also may become fibroblasts, odontoblasts or osteoclasts. Undifferentiated mesenchymal cells constitute a reservoir of cells upon which a body can cell to assume functions that are not ordinarily needed. In the pulp, they are usually found outside the vessel walls. Before injury, they appear elongated and following injury they differentiated into macrophages and as such can ingest foreign material. Characteristically, a macrophage has numerous vesicles, vacuoles and membrane bound bodies known as lysosomes. The lysosomes contain various hydrolytic enzymes that air in breakdown of the ingested material. Other transitional cell forms in the pulp include ameboid cells of various types and lymphoid wondering cells.
  • 21. FIBRES Collagen is the predominant extracellular matrix comprising 25-32% of dry wt and 3.5% of wet wt of pulp. Collagen fibres are synthesized by the pulpal fibroblasts. A single collagen molecule referred to as tropocollagen, consists of 3 polypeptide chains, designated as either a 1 or a 2 depending on their amino acid composition and sequence. The different combinations and linkages of chains making up the tropocollagen molecule have allowed collagen fibres and fibrils to be classified into a number of types. Type I – Found in skin, tendon, bone, dentin and pulp 56% Type II – Found in cartilage Type III – Found in most unmineralized connective tissue Type IV and VIII collagen – components of basement membranes Type V – Constituent of interstitial tissues Type III collagen constitutes 25%-45% of pulp while type I constitutes around 50%. Both type III and type I have a similar 67nm bonding but type I collagen continues both a1 and a2 molecules chains, type III contains only a1 chains. With maturity, collagen fibers of approx 750A0 diameter develop. In young pulp, small collagen fibers stains black with silver impregnation stains. Thus, they are referred to as argyrophilic fibers. Fine argyrophilic fibers arising in the pulp, form spirally twisted bundles that
  • 22. pass between the odontoblasts and fan out into the unmineralized dentin or predentin in a delicate meshwork. These fibers called VAN KROFFS fibers form the fibrillar network of the dentin. There are 2 prominent patterns of collagen deposition in dental pulp. - Diffuse (in which collagenous fibers lack definite orientation). - Bundle type (in which large, coarse bundles run parallel to nerves or independently). Coronal pulp tissue has more bundle collagen diffuse collagen. As the pulp gets older, there is an increase in fiber extent – mainly type III collagen. Regardless of age, the apical portion of the pulp is usually more fibrous than the coronal portion. Clinically, the apical pulp tissue has a whitish appearance due to the predominance of collagen fibers. Once mature collagen is formed, it is less prone to damage. As the pulp chamber narrows with age, the collagens inability to disintegrate to accommodate the smaller lumen results in fibrosis – a congestion that could be called “CRABGRASS” effect. Ground substance : It is dense and gel like in nature, varies in appearance from finely granular to fibrillar with clear spaces left between various aggregates. It is composed of both acid mucopolysaccharides and protein polysaccharide compounds, i.e. glycosaminoglycans and proteoglycans. 20% of the pulpal carbohydrate is in glycosaminoglycans. The following properties have been attributed to glycosaminoglycans. - Water retention - Ion binding and electrolyte distention during mineralization. - Influence on collagen fibrillogenesis.
  • 23. The metabolism of the cells and the fibers of the pulp is mediated through the ground substance. It is a viscid fluid and is described by Engel (1958) as the “milieu interieur” through which metabolites pass from the circulation to the cells and through which breakdown products from the cells come back to venous circulation. Thus, the metabolic role of the ground substance influences the vitality of the pulp. In all, the ground substance, - Influences the spread of infection - Metabolic changes in cells - Stability of crystalloids - Effects of hormones vitamins and other substances Any changes in the nature or quality of the ground substance directly influences the spread of inflammation and infection. 1. Van Hassel has demonstrated that local increases in fluid presence are exactly that – LOCAL-confined to the site of injury or irritation by a resilient connective tissue. The viscosity of the gelated ground substance reinforced with collagen fibers does not permit fluids to move readily from one part of the pulp to another or the presence to be transmitted through the tissue. 2. The gelated ground substance acts as a barrier against the spread of microorganisms and toxic products. However, organisms such as the haemolytic streptococcus can elaborate a spreading factor (the enzyme, hyaluronidase) that may dissolve the barrier and allow a faster invasion. 3. Although the turgidity of the ground substance resists the spread of inflammation, the process moves apically by increments from a particular site. Pressure from the increased tissue fluid collapses the thin
  • 24. walled veins and venules, causing a vascular stasis and ischemia resulting in local cellular death. 4. Chemical mediators (eg. proteolytic enzymes, hyaluromidase) edema, and heat may also alter the quality of the ground substance (hydrolytic agents). 5. Chemotactic factors, chemicals liberated from injured cells not only alter the viscosity but also exert chemotactic influence on PMNL’s and macrophages. 6. The viscosity can be further decreased by an excessive accumulation of inflammatory fluid (edema) and a localized temperature rise, both resulting from inflammation. 7. The temperature alters the state of ground substance in much the same way as in a reversible hydrocolloid, a sol-gel type of interplay. The heat of an inflamed pulp by separating the molecules diminishes the natural barrier of the gelated state. METABOLISM : The metabolic activity has been studied by measuring the rate of oxygen consumption and the production of CO2 or lactic acid by pulp tissue in vitro. Because of the relatively sparse cellular composition of the pulp, the rate of oxygen consumption is low in comparison to that of most other tissues. During active dentinogenesis, metabolic activity is much higher than after the completion of crown development. The greatest metabolic activity is found in the region of the odontoblast layer. In addition to the usual glycolytic pathway, the pulp has the ability to produce energy though a phosphoglyconate shunt type of carbohydrate metabolism, suggesting that the pulp may be able to function under varying
  • 25. degrees of ischemia. This could explain how the pulp manages to withstand periods of vasoconstriction resulting from the use of infiltration anesthesia employing the epinephrine – containing local anesthetic agents. CIRCULATION : The circulation of blood is the transportation system by means of which the various cells of the body are supplied with nutrients and the waste products from the cells are removed for elimination from the body. Systemic circulation : From the venae cavae the blood passes into the right atrium and from there it passes then the right ventricle and into the lungs by way of the pulmonary artery. The blood is oxygenated in the lungs and returns to the heart by way of pulmonary vein, to the left atrium and is pumped through the left ventricle to the aorta. The aorta gives off blood vessels (arteries) that divide into smaller and smaller branches- the arterioles. The arterial supply to the pulps of teeth originates from the posterior superior alveolar, the infaorbital and the inf. alveolar branches of the internal maxillary artery. A single artery or several smaller arteries enter the pulps their the apical foramen or foramina. In addition, numerous smaller vessels enter through lateral and accessory foramina. Blood is returned to the heart by the venous system. The pulpal veins together with other venous tributaries form the pterygoid plexus located posterior to the maxillary tuberosity. The pterygoid plexus drains into internal maxillary vein and this into the external or internal jugular vein – superior vena cava – heart.
  • 26. Microcirculation : The primary function of microcirculation is to transport nutrients to and to remove metabolic waste products from the tissues. the pulp organ is extensively vascularized. Blood from the dental artery enters the tooth via arterioles having diameters of 150µm or less. These vessels pass through the apical foramen or foramina with nerve bundles. Smaller vessels may enter the pulp via lateral or accessory canals. The arterioles course up through the central portion of the radicular pulp and give off branches that spread laterally toward the odontoblast layer, beneath which they cavity to form a capillary plexus. As the arterioles pass into the coronal pulp the fan out toward the dentin, diminish in size and give rise to a capillary network in the subodontoblastic region ranging from 4 to 8µm in diameter. This network provides the odontoblasts with a rich source of metabolites. There is no Tunica media and adventitia in the capillaries. Are made up entirely of a single layer flat endothelial cells that is continuous with the endothelial lining Located on the periphery of the capillaries at random are pericytes or Rouget) Function of these cells is controversial, thought to be contractile cells capable of reducing the size of the lumen. Capillary blood flow in the coronal portion of the pulp is nearly twice that in the root portion. Moreover, blood flow in the region of the pulp horns is greater than in other areas of the pulp. In young teeth, during dentinogenesis, capillaries commonly extend into the odontoblast layer, thus assuring an adequate supply of nutrients for the metabolically active odontoblasts and retreat more pulpally once dentinogenesis is completed. The subodontoblastic capillaries are surrounded by a basement membrane and occasionally fenestrations (i.e. pores) are observed in
  • 27. capillary walls. These fenestrations are thought to provide rapid transport of fluid and metabolites from the capillaries to adjacent odontoblasts. THE SUBODONTOBLASTIC PLEXUS In the efferent venous system : Blood passes from the capillary plexus first into the post capillary venules and then into larger venules. Venules in the pulp have diameter comparable to the arterioles but unusually thin walls which make their lumina large which may facilitate the movement of fluid in or out of the vessels. The muscular coat of these venules is thin and discontinuous. The collecting venules become progressively larger as they course to the central region of the pulp. The largest venules have a diameter of that may reach a
  • 28. maximum of 200mm, thus they are considerably larger than the anterioles of the pulp. Arteriovenous anastomoses (AVA) may be present in both coronal and radicular pulp. Such vessels provide a direct communication between arterioles and venules, thus bypassing the capillary bed. The AVA’s are relatively small venules with a diameter of approximately 10mm. Among the oral tissues, the young and normal pulp has the highest volume of blood flow but it is substantially lower than blood flow in the major visceral organs. Regulation of pulpal blood flow : Pulpal blood flow has been estimated to be 20-60ml /min per 100g of tissue. Chemical regulation : Nerves help to regulate the blood supply to the dental pulp. - Sympathetic (adernregic) nerve fibers liberate norepinephrine which constricts the vessels. - Parasympathetic (cholinergic) nerves liberate acetylcholine which dilates the vessels. The catecholamines such as epinephrine or norepinephrine exert there physiologic effects on receptors in the blood vessels, called “adrenoreceptors”. There are 2 types of adrenoreceptors. - Alpha (α) - Beta (β) The blood vessels of pulp contain both α and β adrenoreceptors. α receptors are responsible for contraction and produce vasoconstriction.
  • 29. Stimulation of β receptors causes a relaxation of the vascular musculature. The pulpal blood vessels contain β adrenoreceptors but are poorly equipped with them. Blood circulation in an inflamed pulp involves very complex pathophysiologic reactions. A unique feature of the pulp is that it is rigidly encased within dentin. This places it is a low-COMPLIANCE environment, much like the brain, nail-bed and bone-marrow. Thus, pulp tissue has limited ability to expand so vasodilatation and increased vascular permeability evoked during an inflammatory reaction results in an increase in pulpal hydrostatic pressure. INNERVATION : The neuron is the basic cell of the nervous system. Like other cells, each neuron has a nucleus and surrounding cytoplasm. The neuron has one relatively long branch – the axon and numerous five branch (dendrites). The axon transmits brief electrical waves called impulses, the dendrites receive nerve impulses from other cells. The pulp is heavily innervated. For eg : appox. 2500 axons enter the apical foramen of a mature premolar. Pulp tissue is innervated by the fibers of sensory division of the trigeminal ganglions and those of autonomic branches of superior cervical ganglion. The principal function of sensory nerves is to detect stimuli and to conduct to the C.N.S. The function of autonomic system is to keep the internal state of the organism constant and maintain homeostasis.
  • 30. The sensory system seems to be well suited for signaling potential damage to the tooth. The tooth is innervated by a large numbero f myelinated and unmyelinated nerve fibers. Meylinated – these have a sheath of myelin, a substance composed largely of fatty substances as lipids. Myelin sheath functions as an insulator – deposited by schwann cells. Unmyelinated – usually found in autonomic nervous system, they accompany blood vessels. Approximately 80% of nerves are unmyelinated. Regardless of the nature of sensory stimulus, almost all afferent impulses from the pulp result in the sensation of pain. The nerve fibers are seen centrally in the pulp of the root in close association with the blood vessels. A few fibers leave the central bundles in the root and travel to the periphery. Most continue to the coronal pulp where they spread apart and branch profusely. Most of the branches are in the odontoblastic or subodontoblastic regions. Once they reach the coronal pulp, they fan out beneath the cell-rich zone, branch into smaller bundles and finally ramify into a plexus of single nerve axons known as PLEXUS OF RASCHKOW. Full development of this plexus does not take place until final stages of tooth development. Branches from this plexus pass into the odontoblastic layer and the predentin to form the MARGINAL PLEXUS, others continue into dentin to accompany odontoblastic process into the dentinal tubules.
  • 31. Ochi and Matsumoto found the approximation of the nerve fibers and dentinoblastic processes to be about 20nm with no gap junctions or synapses present. PLEXUS OF RASCHKOW Nerve endings do not exist in every tubule. Intratubular nerves appear in 10%-20% of the tubules in the coronal pulp horn region, compared with less than 1% at the level of the CE junction and only occasionally nerves are found in radicular dentin. Most of these intratubular fibers extend into the dentinal tubules for only a few mm, but a few may penetrate as for as 100mm.
  • 32. Nerve fibre types : The speed with which a nerve impulse passes along a neuron varies directly with the diameter of the axon the larger the diameter, the faster the conduction. Fibers having the largest diameter are classified as A fibers, intermediate size- B fibers and smallest diameter – C fibers. The A fibers are myelinated and subdivided into the larger diameter – A α and A-β Intermediate - Aγ Smaller – AB Of considerable clinical interest is the evidence that nerve fibers of the pulp are relatively resistant to necrosis. This apparently because nerve bundles, in general, are more resistant to autolysis than other tissue elements. even in degenerating pulps, C fibers might still be able to respond to stimulated. Also, C fibers are able to function in hypoxia, even after blood flow has been compromised. This may offer an explanation as to why instrumentation of non-vital teeth some times causes pain. Also, it has been observed that removal of pulp by extraction of the tooth or by pulpectomy and presumably, pulpotomy results in the successive degeneration of the cell bodies located in the spinal nucleus of the trigeminal nerve, the main sensory ganglion and the peripheral nerve leading to the tooth in the socket. Bernick : observed the effects of caries and restorations on underlying nerves in the pulp. He found a degeneration of subodontoblastic plexus of nerves associated with the production of dentin. He concluded that the terminal nerves in the injured pulp are sensitive to the noxious products of
  • 33. caries and the restorative procedures. The lack of sensitivity that accompanies the caries process may be attributable, at least partially, to degeneration of underlying nerves. Vitality testing: ELECTRIC PULP TESTER delivers a current sufficient to overcome the resistance of enamel and dentin and stimulate the sensory A fibers at the pulp-dentin border zone. C fibers of the pulp do not respond to the conventional pulp tester because significantly more current is needed to stimulate them. Bender et al found that in anterior teeth, the optimal placement site of the electrode is the incisal edge of anterior teeth, as the response threshold is the lowest at that location and increases as the electrode is moved toward the cervical region of the tooth. Cold tests using CO2 snow or liquid refrigerants and heat tests employing heated gutta percha or hot water activate hydrodynamic forces within the dentinal tubules which in turn excite the interdental A fibers. C fibers are not activated by these tests unless they produce injury to the pulp. It has been shown that cold tests do not injure the pulp. Heat tests have a greater potential to produce injury, but if the tests are used properly, injury is not likely. Neuropeptides : Of immense current interest is the presence of neuropeptides in sensory nerves. Pulpal nerve fibers contain neuropeptides such as calcitonia gene-related peptide (CGRP), substance P (SP), neuropeptide Y, neurokinin A and vasoactive intestinal polypeptide (VIP). Release of these peptides can be triggered by such things as tissue injury, complement activation, antigen antibody reactions nerve.
  • 34. Once released vasoactive peptides produce vascular changes that are similar to those evoked by histamine and bradykinin (i.e. vasodilatation). In addition to their neurovascular properties, SP and CGRP contribute to hyperalgesia and promote wound healing. LYMPHATICS : The existence of lymphatics in the pulp has been a matter of debate because it is not easy to distinguish between venules and lymphatics in ordinary light micrope techniques. However, techniques using light and electron microscopy have described lymphatic capillaries in human pulp. Their fine endothelial structure makes them difficult to see. Main function of these lymphatic vessels is : - Removal of interstitial fluid and metabolic waste products. - To maintain the intrapulpal tissue pressure at a normal level (10mm of Hg). These lymphatic vessels follow the course of venules toward apical foramen. Lymph vessels consist of endothelial lined channels with discontinuities in their walls and basement membrane. They are characterized by the absence of RBC’s and presence of lymphocytes. Lymph vessels draining pulp and periodontal tissues have a common outlet. They drain into submental, submandibular, and deep cervical lymph nodes and finally – junction of subclavian and Internal jugular veins.
  • 35. REGRESSIVE AND AGE CHANGES : Regressive : The term regressive is defined as a condition of decreased functional capability or of returning to a more primitive state. Older pulps have been described as regressive and as having a decreased ability to combat and recover from injury. This is because older pulps have fewer cells, a less extensive vasculature and increased fibrous elements. Cell changes : In addition to the appearance of fewer cells in aging pulp, the cells are characterized by a decrease in size and number of cytoplasmic organelles. The fibroblast of an aging pulp exhibits less perinuclear cytoplasm and passes long, thin cytoplasmic processes. The intracellular organelles are also reduced in size and number, the mitochondria and endoplasmic reticulum being good examples of this. Fibrosis : The increase in fibers in the pulp organ is gradual and generalized throughout the organ. Any external trauma such as dental caries or deep restorations usually causes a localized fibrosis or scarring effect. The increase in collagen fibers may be more apparent than actual, due to the decrease in size of the pulp. Which makes the fibers occupy less space, and hence may become more concentrated without increase in total volume. Vascular changes : Occur in the aging pulp as they do in any organ. Arthrosclerotic plaques may appear in pulpal vessels. In other cases, the outer diameter of
  • 36. vessel walls becomes greater as collagen fibers increase in the medial and adventitial layers. CALCIFICATIONS : Calcifications are also found commonly surrounding blood vessels. Basically, there are 2 distinct types of calcifications. 1) Formed structures – commonly called as pulp stones or denticles. 2) Tiny crystalline masses generally termed diffuse calcifications. Pulpstones are found predominantly in the coronal portion whereas calcifications are found in radicular pulp seems to be of diffuse variety. Pulp stones : Pulpstones or denticles are diffuse, or nodular, calcified masses appearing in either or both the coronal and root portions of the pulp organ. They usually are asymptomatic unless they impinge on nerve and blood vessels. They have been seen in functional as well as erupted teeth. Pulp stones range in size from small, microscopic particles to accretions that occupy almost the entire chamber. I. According to their structure, they have been classified as - True denticles - False denticles II. According to the location - Free - Attached - Embedded
  • 37. True denticles : They are similar in structure to dentin, in that they have dentinal tubules and contain the processes of odontoblasts that formed and that exist on their surface. True denticles are comparatively rare and are usually located close to the apical foramen. A theory has been advanced that the development of the true denticle is caused by inclusion of remnants of the epithelial root sheath within the pulp. The epithelial remnants induce the cells of the pulp to differentiate into odontoblasts, which then form the dentin masses called the pulp stones. They do not exhibit dentinal tubules but appear instead as concentric layers of calcified tissue. In some cases, these calcification sites appear within a bundle of collagen fibers. Other times, they appear in a location in the pulp free of collagen accumulations. Some false pulp stones undoubtedly arise around vessels. In the center of these concentric layers of calcified tissue, there may be remnants of calcified and necrotic cells. calcification of thrombi in blood vessels, called “PHLEBOLITHS” may also
  • 38. serve as vili for false denticles. All denticles begin as small nodules but increase in size by incremental growth on their surfaces. The surrounding pulp tissue may appear quite normal. Pulp stones may eventually fill substantial parts of the pulp chamber. FREE STONES are islands entirely surrounded by pulp tissue. ATTACHED DENTICLES are partly fused with the dentin. EMBEDDED DENTICLES are entirely surrounded by dentin. All are believed to be formed free in the pulp and later to become attached or embedded as dentin forma. Progresses pulp stones may appear close to blood vessels and nerve trunks. Only a relatively small member of pulp stones are sufficiently large enough to be detected in radiographs. The incidence, as well as the size of pulp stones increases with age. According to one estimate : 66% - 10-30yrs 80% - 30-50 yrs 90% - over 50 yrs HISTOLOGICALLY : 2 types of stones are recognized 1) Those that are round or ovoid, with smooth surfaces and concentric lamellations. 2) Those that assume no particular shape, lack laminations and have rough surfaces. Laminated stones appear to grow by the addition of collagen fibrils to their surfaces, whereas unlaminated stones develop via the mineralization of preformed collagen fiber bundles.
  • 39. FUNCTIONS OF PULP : Inductive : The primary role of the pulp is to interact with the oral epithelium cells, which leads to differentiation of the dental lamina and enamel organ formation. The pulp also interacts with the developing enamel organ as it determines a particular type of tooth. Formative : The pulp organ cells produce the dentin that surrounds and protects the pulp. The pulpal odontoblasts develop the organic matrix and function in its calcification. Through the development of the odontoblast processes, dentin is formed along the tubule wall as well as at the pulp-dentin front and this process continues throughout the life of the tooth. Nutritive : The pulp nourishes the dentin through the odontoblasts and their processes and by means of the blood vascular system of the pulp. Protective : The sensory nerves in the tooth respond with pain to all stimuli such as heat, cold, pressure, operative cutting procedures and chemical agents. The nerves also initiate reflexes that control circulation in the pulp. This sympathetic function is a reflex, providing stimulation to visceral motor fibers terminating on the muscles of the blood vessels. Defensive or reparative : The pulp is an organ with remarkable reparative abilities. It responds to irritation, whether mechanical, thermal, chemical or bacterial by producing reparative dentin and mineralizing any affected dentinal tubules. Both the reparative dentin created in the pulp and the calcification of the
  • 40. tubules (sclerosis) are attempts to wall off the pulp from the source of irritation. Also, the pulp may become inflamed due to bacterial infection or by cutting action and placement of an irritating restorative material. The pulp has macrophages, lymphocytes, neutrophils, monocytes and plasma and mast cells, all of which aid in the repair of the pulp. PULPAL PATHOLOGY: As I mentioned before, the pulp is a connective tissue, as found elsewhere in the body. However, several factors make it unique and thus alter its ability to respond to irritation : 1) The pulp is almost totally surrounded by a hard tissue (dentin), which limits the area for expansion and restricts the pulp’s ability to cope with bacteria, necrotic tissue and inflammation. 2) The pulp possesses a unique cell, the odontoblast, as well as cells that can differentiate into hard tissue-secreting cells that form more dentin and / or irritation dentin in an attempt to protect the pulp from injury. 3) The pulp has almost a total lack of collateral circulation which severely limits its ability to cope with bacteria, necrotic tissue and inflammation. In spite of these circumstances, studies have indicated that an injured pulp has some capacity to recover, but the degree is uncertain.
  • 41. CLINICAL CONSIDERATIONS : The causes of pulp inflammation, necrosis and dystrophy, beginning with the most frequent irritant, micro-organisms are: Iatral causes : Cavity preparation : The heat generated by grinding procedures of tooth structure has often been cited as the greatest single cause of pulp damage during cavity preparation. Swerdlow and Stanley pointed out the basic factors in rotary pointed out the basic factors in rotary instrumentation that cause temperature rise in the pulp. In order of their importance : 1) FORCE applied by the operator 2) SIZE, SHAPE and CONDITION of the cutting tool 3) Revolutions per minute 4) DURATIONS of actual cutting time We are bound to think that the ultraspeed (30,000 rpm) instruments of today are more traumatic to the pulp than the low speed (6,000 rpm) instruments of the past. This is not true, if adequate air-water coolant is used. It is possible to “burs” the pulp in 11 seconds of preparation time if air alone is used as coolant at 200,000 rpm. It should be remembered that the highest intrapulpal temperatures are reached within the first 10 seconds of grinding. Studies have concluded that the demise of the pulp begins with a chronic lesion turned acute by the insult of cavity preparation. An increase in interpulpal temperature of 200 F may result in irreversible damage. Also, carbide burs generate less thermal change than diamond instruments and
  • 42. among the diamond burs – coarse diamonds produce a more pronounced temperature increase than fine diamonds. Depth of the preparation is also an important factor. Deeper the penetration, more is the pulp damage. The degree of pulp response is inversely proportional to the remaining thickness of dentin. Pulp horn extensions are a very important consideration. The close proximity of the pulp to the external surface of the tooth leads to exposure if the pulp horn is not taken into consideration during cavity cutting. At some points, the pulp is only 1.5 to 2.0mm away before preparation is even begun. Sproles in a study reported that 66-96% of the time in the 1st and 2nd molar teeth the cervical pulp horns presents a real danger in cavity preparation. PERIODONTAL STATUS AND PULP : There is an intimate relationship between the periodontal vascular plexus and the pulpal blood vessels. Besides vascular communication, connective tissue fibers run from the dental pulp to the periodontal ligament. Inflammatory lesions in the pulp may be responses to toxic products entirely through canal openings that normally are covered with bone and periodontal but now are exposed to oral fluids. Pulpal inflammation in periodontally involved teeth can occur from extension of the inflamed periodontal connective tissue. Gingival recession may expose the opening. Also deep scaling and currettage in periodontal treatment may possibly be instrumental in causing pulp damage. Sensitivity of the teeth after deep scaling and curettage may
  • 43. be due not only to denudation of the roots of the teeth but also to the production of inflammatory changes or haemorrhages in the pulps of the teeth. During curettage of a periodontal lesion that extends entirely around the apex of the root, the pulp vessels may be severed and the pulp devitalized, of a lateral root canal, especially in the furcation area, causing pain and possible spread of infection into the pulp. ORTHODONTIC FORCE AND PULP : In theory, the application of light sustained force to the crown of a tooth should produce a periodontal reaction but share little, if any, effect on the pulp. There is probably a modest and transient inflammatory response within the pulp, at least at the beginning of the treatment. There are occasional reports of tooth vitality during orthodontic treatment. Poor control of orthodontic force could be the culprit. If a tooth is subjected to heavy, continuous force, a sequence of abrupt movement occurs. A large enough abrupt movement of the root apex could severe the blood vessels as they enter. As proof that orthodontic tooth movement does affect pulp viability. Hamersky and colleagues found 27% depression in pulp tissue respiration as a result of orthodontic force application. Tooth preparations for crowns require removal of most of tooth enamel. Dentinal tubules are opened by the tooth preparation and the prepared teeth are more susceptible to dehydration. Minimal tooth drying is suggested to avoid pulpal damage from tooth dehydration. It is mandatory that all crowns and fixed prosthesis are checked for occlusion while seating, thus eliminating the problem of occlusal prematurities.
  • 44. Preparation in vital dentin usually makes use of local anesthesia necessary. As a result, the appropriate nerve mediated vascular responses to the preparation trauma will be attenuated for a while. This is not regarded as a serious problem. Because pulpal never are only blocked for a few minutes after injection. However, when a vasoconstrictor (epinephrine /adrenaline) is used, there will be a long lasting period of reduction in basal blood flow. Infiltration anesthesia in upper front tooth region may lower blood perfusion of the pulp in adjacent teeth by 70-80% for more than 1hour. These changes are not as prominent with a mandibular block but the pulp is likely to be vulnerable to the clinical procedures directed to tooth structure. It is therefore advisable to avid catecholamine vasoconstrictor when preparing for restorations in teeth with vital pulp.
  • 45. THE FUTURE : Pulp death seems to be on the increase, or perhaps only an apparent increase owing to an awareness of the value of the treated pulpless tooth. With routine examination and early treatment, with a cautious temperate approach to all restorative procedures and with a sensible use of filling materials, the dentist can prevent a great deal of pulp death. Prevention of pulp injury: The “dentistogenic” or iatrogenic cause accounts for an embarrassingly high percentage of the pulp injury and death reflected in the A.D.A. report. The university of Connecticut reported that “previous restorative treatment” was the major etiologic factor leading to root canal therapy. There are many day-to-day insults leried against the pulp that can be prevented. 1) Depth of cavity and crown preparation. 2) Width and extension of cavity and crown preparation. 3) Heat damage and dessication during cavity preparation. 4) Chemical injury through medicaments 5) Toxic cavity liners and bases 6) Toxic filling materials 7) Prevention of microleakage Recent advances: Pulp cells may hold the key to treatment in Parkinsons disease. - A study in may issue of European journal of neuroscience shows dental pulp cells provide great support for nerve cells lost in
  • 46. Parkisons disease and could be transplanted directly into the affected parts of the brains. - This study was the first to test the post-natal stem cells from the more readily available tooth pulp in the nervous system. - “Noscat” has also studied dental pulp stem cells as a treatment for spinal cord injuries. - However, many years are left for this therapy to be treated in people for cure. CONCLUSION : It is to correlate clinical practice with basic science because ultimately, an underpinning of basic sciences leads to the most effective clinical treatment “Dentistry without basic sciences is only a craft but with good foundation in these sciences, it is a learned profession”. As heart is to the body, the pulp is to the tooth, providing a constant source of nutrition to maintain the vitality of a tooth. Every precaution should be taken to preserve vitality of the pulp.
  • 47. REFERENCES : - Stephen Cohen “Pathways of pulp” 8th edn - John Ingle “Endodontics” 5th edn - Orbans “Oral Histology” - Seltzer “The dental pulp” 2nd edn - “Review of dental pulp – Clinical considerations”. Quintessence Int 1982: 135-137.