dental pulp by pedodrrahulmishra

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									INTRODUCTION

       A tooth has four main components- enamel, dentin, pulp and

the cementum. Dental pulp is the central most component of the

teeth which makes the tooth a living entity due to the rich

vascularity and innervation.



       However,   a    close   relationship      between   the    odontoblasts

lining, the periphery and the dentin is the reason why pulp-dentin

complex is considered as a functional entity.



       As pulp imparts life to the tooth so it becomes more

important to have a thorough knowledge regarding pulp so as to

have a thorough knowledge of a healthy dentition in toto.



DEFINITIONS OF DENTAL PULP:

       According to Dorland‟s illustrate of medical dictionary dental

pulp   is   defined    as   the   richly    vascularized    and        innervated

connective    tissue   contained    in     the   pulp   cavity    of    a   tooth,

constituting the formative, nutritive and sensory organ of the

dentin; called also as pulpa dentis.



       According to Harty and Rogston concise illustrated dental

dictionary pulp is defined as a soft mass of tissue and pulp in

dentistry, soft tissue lying within the dentine of a tooth and

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containing fibers, cells and structures such as blood vessels,

sensory nerves and lymphatics. These vessels pass through the

apical foramen of the tooth or through accessory canals.



     According to Jablonski‟s illustrated dictionary of dentistry

dental pulp is a richly vascularized and innervated connective

tissue of mesodermal origin, contained in the central cavity of a

tooth and delimited by the dentin, and having formative, nutritive,

sensory and protective functions. The portion housed in the tooth

chamber proper is known as coronal pulp; that within the root as

radicular pulp.



     According to Cohen and Burn pulp is a soft tissue of

mesenchymal origin residing within the pulp chamber and root

canals of the teeth.



FUNCTIONS OF DENTAL PULP

1.   Formative:

     The main function of pulp is the formation of dentine. From

the mesodermal aggregation known as dental papilla arises a

specialized cell layer of odontoblasts adjacent and internal to the

inner layer of the ectodermal enamel organ. Ectoderm interacts

with mesoderm and the odontoblasts initiate the process of dentin

formation.

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2.   Nutritive:

     It supplies nutrition to the dentin through blood vessels and

odontoblastic processes and maintains vitality of tooth.



3.   Sensory:

     Innervation of the pulp and dentin is linked by the fluid and

by its movement between the dentinal tubules and peripheral

receptors and thus to the sensory nerves of the pulp proper. The

sensation of the tooth is felt through the nerves of the pulp.



4.   Defensive:

     Defense of the tooth and the pulp itself has been speculated

to occur by creation of new dentin in the face of irritants.



DEVELOPMENT OF DENTAL PULP:

     Pulp is derived from the cephalic neural crest. Neural crest

cells arise from the ectoderm along the lateral margins of neural

plate and migrate extensively. Those that travel down the sides of

the head into the maxilla and mandible contribute to the formation

of the tooth germs. The dental papilla, from which the pulp arises

develops   as ectomesenchymal cell      proliferation   and condense

adjacent to the dental lamina at the sites where teeth will develop.




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     Pulp formation starts on the eighth week of the intra-uterine

life in the region of incisors. First there is proliferation and

condensation of mesenchymal elements known as dental papilla.

The epithelial elements proliferate rapidly and assume a bell shape

and enclose the future pulp tissue. Maturation of the dental papilla

progressively moves apically, beginning at the tooth‟s most coronal

level and on its apex. By the time a tooth erupts, the pulp within

could arbitrarily termed as „mature‟. Along with development, pulp

becomes vascular and star shaped fibroblasts develop.


ANATOMY OF PULP CAVITY IN PRIMARY DENTITION

Maxillary central incisor:

     Pulp cavity of this tooth follows general outline, although the

pulp horns are larger and more pointed than the external form

would suggest. There is no dermarcation of the pulp cavity into a

separate pulp chamber and root canal.


Maxillary lateral incisor:

     The pulp cavity generally conforms to the surface contours of

the tooth.


Maxillary primary cuspid:

     The pulp cavity follows closely the external crown form.

Therefore, there are three pulp horns mesial, central and distal.

The central horn is the longest and the mesial the shortest. The

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pulp canal of the maxillary primary cuspid shows a marked

constriction to the apical third of the root.


Maxillary first molar:

      The pulp chamber follows the external crown form with a pulp

horn projecting into each cusp. The mesiobuccal pulp is the

largest, the mesiolingual next and the distobuccal the smallest. The

apices of both the mesiobuccal and mesiolingual pulp horns are

located toward the mesial wall of the pulp chamber. Three root

canals extend from the pulp chamber. The orifices of the canals are

located in the floor of the pulp chamber near the mesiobuccal and

distobuccal angles and the lingual wall of the chamber.


Maxillary second molar:

      The pulp cavity is formed by the pulp chamber and three root

canals which correspond to the surface form of the teeth. There are

four pulp horns which extend from the occlusal wall. A fifth horn

may arise from the middle third of the lingual wall and extend

toward the occlusal. The mesiobuccal horn is the largest and

longest of the pulp horns forming a considerable portion of the

pulp cavity. The apex of the horn is quite pointed and extends to

the   mesial   and   buccal.   The       distobuccal,   mesiolingual   and

distolingual pulp horns correspond in relative size to the cusps

which they occupy with the distolingual being the smallest.


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Mandibular central incisor and lateral incisor:

     Pulp cavity conforms to general surface contour of the tooth.



Mandibular cuspid:

     The pulp cavity closely follows the surface contour form.

There is no differentiation between the pulp chamber and the root

canal. The root canal terminates with an abrupt constriction at the

apical foramen.



Mandibular first molar:

     The pulp cavity is formed by pulp chamber which occupies

the coronal portion of the tooth and pulp canals. The general form

of the pulp chamber conforms roughly to the surface form of the

crown. There are four pulp horns, the largest bring mesiobuccal

pulp horn which forms a considerable portion of the pulp chamber.

The mesiolingual pulp horn is second smallest in overall height but

third in overall size. The distobuccal pulp horn is second in overall

size. The smallest is the distolingual pulp horn. The floor of the

pulp chamber is arched in the mesiodistal direction, sloping toward

the orifices of the mesial and distal pulp canals, two of which lie in

the mesial root. The third canals lies within the distal root, it is

broad buccolingually and fine mesiodistally.




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Mandibular second molar:

     Pulp cavity is formed by the pulp chamber occupying coronal

portion of the tooth and three pulp canals which are lying in the

root. The form of the pulp chamber corresponds to that of the

crown having five pulp horns. The mesiobuccal and mesiolingual

pulp horns are about equal in height, the distobuccal and

distolingual pulp horns are also approximately equal in height but

are only approximately to-thirds the height of the two mesial pulp

horns, the distal pulp horn is the shortest and the smallest. The

pulp chamber is widest at the mesial; the buccal and lingual

borders converge as they extend toward the distal. The floor of the

pulp chamber is arched in a mesio-distal direction sloping toward

the orifices of the mesial and distal pulp canals.



MORPHOLOGIC ZONES OF THE PULP:

a.   Odontoblast layer:

     The outermost stratum of cells of the healthy pulp is the

odontoblast layer. This layer is located immediately subjacent to

the predentin. Since the odontoblast processes are embedded

within the dentinal tubules, the odontoblast layer is composed

principally of the cell bodies of the odontoblasts. Additionally,

capillaries and nerve fibers may be found among the odontoblasts.




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     In the coronal portion of a young pulp the odontoblasts

assume a tall columnar form. The tight packing together of these

tall slender cells produces the appearance of a palisade. The

odontoblasts vary in height, consequently, their nuclei are not all

at the same level and are aligned in a staggered array often

producing the appearance of a layer three to five cells in thickness.

Between   odontoblasts    there   are   small   intercellular   spaces

approximately 300 – 400 in width.



     The odontoblast layer in the coronal pulp contains more cells

per unit area than in the radicular pulp. The odontoblasts in the

coronal pulp are usually columnar whereas those in the midportion

of the radicular pulp are more cuboidal. Near the apical foramen

the odontoblasts appear as a flattened cell layer. Since 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. The cell body of most of the

odontoblasts borders on the predentin, however the odontoblast

processes pass through the predentin into the dentine.



     Between adjacent odontoblasts there are three types of

specialized cell to cell junctions (Holland, 1975; Holland, 1976;

Koling, 1988).


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     i.     Spot desmosomes (Macula adherens): Located in the

            apical part of odontoblast cell bodies mechanically join

            odontoblasts together.

     ii.    Gap junctions (Nexusex): Numerous nexuses provide

            low   resistance   pathways    through   which   electrical

            excitation   can   pass    between   odontoblasts.   These

            junctions are most numerous during the formation of

            primary dentine. Gap junction and desmosomes have

            also been observed joining odontoblasts to the processes

            of fibroblasts in the subodontoblastic area.

     iii.   Tight junctions (Zonula occludens): Are found mainly

            in the apical part of odontoblasts in young teeth. These

            structures consist of linear ridges and grooves which

            close off the intercellular space. It appears that tight

            junctions determine permeability of the odontoblast

            layer by restricting the passage of molecules ions and

            fluid between the extracellular compartments of the

            pulp and predentin.



b.   Cell-poor zone (Peripheral zone):

     Immediately subjacent to the odontoblast layer in the coronal

pulp there is often a narrow zone approximately 40 m in width

that is relatively free of cells. It is traversed by blood capillaries,


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unmyelinated nerve fibers and the slender cytoplasmic processes of

fibroblasts. The presence or absence of the cell-poor zone depends

upon the functional status of the pulp. It may not be apparent in

young pulps rapidly forming dentin or in older pulps where

reparative dentin is being produced.



c.    Cell-rich zone:

      Usually        conspicuous      in    the   subodontoblastic    area   is   a

stratum containing as relatively high proportion of fibroblasts

compared with more central region of the pulp. It is more

prominent      in      coronal     pulp    than   in   radicular   pulp.   Besides

fibroblasts,        this    zone   includes     number    of   macrophages    and

lymphocytes.



d.    Pulp proper (Central zone):

      This is the central mass of the pulp. It contains larger blood

vessel and nerves. The connective tissue cells in this zone are

fibroblasts or pulpal cells.



STRUCTURAL ELEMENTS OF THE PULP:

Structural elements of the dental pulp can be classified into;

               a.          Cellular components

               b.          Extracellular components


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a.   Cellular components:

     i.    Odontoblast: It is the most characteristic cell of the

           dentin pulp complex. Each of the odontoblast produce a

           matrix composed of collagen fibers and proteoglycans

           that is capable of undergoing mineralization.

     ii.   Odontoblast process: Cytoplasmic microtubules extend

           from the cell body into the odontoblast process. These

           straight structures follow a course that is parallel with

           the long axis of the cell. Although their precise role is

           unknown theories as to their functional significance

           suggest that they may be involved in cytoplasmic

           extension, transport of materials or simply provision of

           a structural framework (Trowbridge and Kim, 1997).



                Microtubules and microfilaments are the principal

           ultrastructural component of the odontoblast process

           and its lateral branches (Holland, 1985).



                The extent to which the odontoblast process,

           extends outward in the dentin has been a matter of

           considerable controversy. Many ultrastructural studies

           (Brannstrom and Garberoglio, 1972; Holland, 1976;

           Thomas, 1979) have described odontoblast process as

           being limited to inner third of dentin. However Sigal et

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       al., 1984 using antibodies directed against microtubules

       have demonstrated immunoreactivity throughout the

       dentinal tubule suggesting that the odontoblast process

       extends throughout the entire thickness of dentin.

       Obviously, this warrants further study as it is of

       considerable clinical importance to establish the extent

       of the odontoblastic process in human teeth to estimate

       the impact of high speed drilling and other restorative

       procedures on the underlying odontoblast layer.



iii.   Fibroblasts: Although distributed throughout the pulp,

       they are particularly abundant in the cell-rich zone.

       Fibroblasts in the pulp appear to be tissue specific cells

       capable of giving rise to cells that are committed to

       differentiate as odontoblasts, given proper signal. These

       cells are also responsible for producing matrix and

       collagen fibers of the pulp.



            Fitzgerald et al., 1990 demonstrated that mitotic

       activity preceding the differentiation of replacement

       odontoblasts    appear     to   occur   primarily   among

       fibroblasts. Thus, it appears that pulpal fibroblasts.

       Thus, it appears that pulpal fibroblasts can be regarded

       as odontoprogenitor cells.

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iv.     Macrophage        (Histiocytes):    These      cells    are    present

        throughout the connective tissue of the pulp and are

        responsible for phagocytosis. In addition they also

        participate in immune responses and also produces

        interleukin 1 and other cytokines.

v.      Dendritic     cell:   Like     macrophages          they      are   also

        accessory cells of immune system and are also weakly

        phagocytic.

vi.     Lymphocytes: Hahn et al. (1989) have reported finding

        T. lymphocytes and B lymphocytes in normal pulps from

        human teeth. The presence of macrophages, dentritic

        cells   and   lymphocytes        indicate    that      pulp    is   well

        equipped with cells required for the initiation of immune

        responses.

vii.    Mesenchymal cells (Reserve cells): These are present

        in   the   cell   rich    zone     and      capillaries       and   are

        pleurepotent in function.

viii.   Mast    cells:    These   cells    are   widely     distributed       in

        connective tissue, where they occur in small groups in

        relation to blood vessels Farnoush (1984) reported the

        presence of mast cells in inflamed as well as uninflamed

        human pulps. The granules of mast cells contain




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          heparen, an anticoagulant, as well as histamine, an

          inflammatory mediator



b.   Extracellular components:

     i.   Ground substance: It is a matrix that makes up the

          bulk of the pulp in which cells and fibres are embedded.



                  Ground substance is a gel0like substance and this

          property may help to limit the spread of bacteria

          (Trowbridge and Kim, 1997).



                  The principal molecular components of interstitial

          ground substance are proteoglycans and glycoproteins.

          In   the      pulp        the    principal     proteoglycans    include

          hyaluronic acid, dermatan sulfate, heparan sulfate and

          chondroitin sulfate.



                  The consistency of a connective tissue such as the

          pulp     in    largely          determined     by    the   proteoglycan

          components           of    the        ground   substance.    The     long

          polysaccharide chains of the proteoglycan molecules

          form relatively rigid coils constituting a network that

          holds      water.     Thus        forming      of   characteristic   gel.

          Hyaluronic acid in particular has a strong affinity for

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      water and is major component of ground substance. The

      water content of the pulp is very high (approximately

      90%) and thus ground substance forms a cushion

      capable of protesting cells and vascular components of

      the tooth.



           Degradation of ground substance can occur in

      certain inflammatory lesion in which there is high

      concentration      of   lysosomal     enzymes         proteolytic

      enzymes; hyaluronidases and chondroiton sulfatases of

      lysosomal as well as bacterial origin are examples of

      hydrolytic enzymes that can attack components of

      ground substances. The pathways of inflammation and

      infection    are   strongly   influenced   by   the    state   of

      polymerization of the ground substance components.



ii.   Fibres of the pulp: Two types of structural proteins are

      found in the pulp colagen and elastin. Elastin fibers are

      confined to the walls of arterioles and unlike collagen

      are not a part of the intercellular matrix.



           The highest concentration of thee fiber bundle is

      usually found in the radicular pulp near the apex. Thus

      Torneck (1985) has advised that during pulpectomy, if

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             the pulp is engaged with a barbed broach is the region

             of the apex this generally affords the best opportunity to

             remove it intact.


      iii.   Innervation:    Pulp    is   a   sensory    organ   capable     of

             transmitting information from its sensory receptors to

             the central nervous system. Regardless of the nature of

             the sensory stimulus (i.e., thermal change, mechanical

             deformation, injury to the tissues) all afferent impulses

             from the pulp result in the sensation of pain. The

             innervation of the pulp includes both afferent neurons,

             which conduct sensory impulses and autonomic fibers,

             which     provide      neurogenic     modulation       of      the

             microcirculation and perhaps regulate dentinogenesis

             too.


CLASSIFICATION OF NERVE FIBERS

Type of fiber           Function               Diameter       Conduction
                                                 (m)       velocity (m/sec)
     A-        Motor proprioception            12-20           70 – 120
     A-        Pressure touch                    5-12           30 – 70

     A-        Motor to muscle spindles          3-6            15 – 30
     A-        Pain, temperature touch           1-5             6 – 30
      B         Preganglionic acetono              <3             3 – 15
C dorsal root   Pain                             0.4-1            0.5 – 2
Sympathetic Postganglionic sympathetic           0.3-1.3         0.7 – 2.3



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        Most of the nerves of the pulp fall into 2 main categories, A -

and C-fibers. The principal characteristics of these fibers are

summarized as follows;

                        Location of                Pain             Stimulation
Fiber   Myelination
                         terminals            characteristics        threshold
                      Principally       in
 A-        Yes       region     of   pulp Sharp, pricking       Relatively low
                      dentin junction
                      Probably                Burning, aching,   Relatively       high,
  C         No        distributed            less bearable than usually associated
                      throughout pulp        A- fiber sensation with tissue injury



        During the bell stage of tooth development, „pioneer‟ nerve

fibers enter the dental papilla following the path of blood vessels

(Fearnhead, 1961). The sensory nerves of the pulp arise from the

trigeminal nerve and pass into the radicular pulp in bundles via

the foramen in close association with arterioles and venules with

the completion of root development the myelinated fibers appear

grouped in bundles in the central region of the pulp. Most of the

unmyelinated C fibers entering the pulp are located within these

fiber bundles, the remainder are situated toward the periphery of

the pulp (Reader and Foreman, 1981).



        Fuss (1986) has found out that the member of A-fibers

gradually increase five years after eruption. The relatively rate



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appearance of A fibers in h pulp helps to explain why he electric

pulp test tends to be unreliable in young teeth.



       The nerve bundles pass upward through the radicular pulp

together with blood vessels. Once they reach the coronal pulp, they

fan out beneath the cell-rich zone, branch into smaller bundles and

finally ramify into plexus of single nerve axons known as the plexus

of Raschkow. Full development of this plexus does not occur until

the final stage of root formation. It has been estimated that each

fiber entering the pulp sends at least eight branches to the plexus

of   Raschkow.     There   is    prolific   to   the   plexus,   producing   a

tremendous overlap of receptor fields (Harris and Griffin, 1968). It

is in the plexus, that the A-fibers emerge from their myelin sheaths

and while still within Schwann cells, branch repeatedly to form the

odontoblastic plexus.



       With the exception of intratubular fibers, dentin is totally

devoid of sensory nerve fibers. This offers an explanation as to why

pain   producing    agents      such   as   acetylcholine    and   potassium

chloride do not elicit pain when applied to exposed dentin.

Similarly, application of topical anesthetic solution to dentin does

not decrease its sensitivity.




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        Pulpal    nerve      fibers   contain           neuropeptides         such     as

neuropeptide Y, calcitonin gene-related peptide (CGRP), vasoactive

intestinal polypeptide (VIP), tyrosine hydroxylase and substance P.

Release of these peptides can be triggered by tissue injury, antigen-

antibody reactions or stimulation of inferior alveolar nerve. Once

released, vasoactive peptides produce vascular changes that are

similar to those evoked by histamine and bradykinin.



        The electric pulp tester delivers current sufficient to stimulate

A- fibers. C-fibers don‟t respond to conventional pulp tester as

more current is required to stimulate them.



        England et al. (1974) showed that nerve fibers of the pulp are

resistant to necrosis. This is apparently due to the fact that nerve

bundles     in   general    are    more     resistant       to    autolysis    even     in

degenerating      pulps,     the    nerve      fibers    could     still   respond      to

stimulation as C-fibers remain excitable even in hypoxia when

blood    flow    has   been     compromised.         This    is    the     reason    why

instrumentation        of   root   canals      of   apparently       non-vital       teeth

sometimes elicit pain.



Comparisons of primary and permanent teeth:

        Number of myelinated and unmyelinated nerve fibers entering

primary     anterior    teeth      have   been      established       (Johnsen        and

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Karlsson, 1974). Fully developed primary canines have more

myelinated and unmyelinated nerve fibers entering than do mature

permanent    canines   and    permanent    incisors,   but   fewer   than

premolars.   The    fully    developed   primary   canine     thus   had

approximately the same capacity to transmit impulses as do single

rooted permanent teeth. The primary incisor has significantly fewer

myelinated and unmyelinated axons entering at the apex than

other teeth with the initiation of root resorption, the number of

nerve fibers significantly decrease.



     Thus, the pain reception, transmission and perception for

primary teeth compared to permanent teeth is different because of

the difference in innervation levels of different teeth as well as

possible difference in receptor mechanisms and interpretation of

impulses as painful by the child as compared to the adult.



Accessory canals:

     During formation of root sheath a break develops in the

continuity of the sheath producing a small gap corresponding to

which dentinogenesis doesn‟t take place thereby giving rise to

accessory canals. It has been shown that number of accessory

canals present in the external furcation area is more than that

present in the internal furcation area. Also pulp canals in primary

dentition are ribbon shape and as infection passes through least

                                   20
resistance therefore radiolucency is seen in the furcation area in

infection.


      iv.    Vascular supply: Blood from the dental artery enters

             the tooth via arterioles having diameters of 100 m or

             less. These vessels pass through the apical foramina in

             company with nerve bundles. Smaller vessels may enter

             pulp via accessory canals.



                    Capillary blood flow in the coronal portion of the

             pulp is nearly twice that in the root portion. Also, blood

             flow in the region of pulp horns is greater.



                    Blood circulation in an inflamed pulp involves very

             complex pathophysiologic reactions. A unique feature of

             pulp is that it is rigidly encased within dentin, thus

             pulp    tissue     has   limited      ability   to   expand,   so

             vasodilatation     and      increased    vascular    permeability

             evoked during an inflammatory reaction results in

             increase in intrapulpal pressure. So any sudden rise in

             intrapulpal      pressure     would     be   distributed   equally

             within the area of pressure increase including the blood

             vessels. Therefore, the thin walled venules become

             compressed thereby increasing vascular resistance and


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            reduction in pulpal blood flow. This is why injection of

            vasodilators such a bradykinin into an artery leading to

            pulp results in reduction rather than increase in pulpal

            blood flow (Kim et al., 1982). Torbejork and Hanin

            (1973) have showed that a reduction in pulpal blood

            flow results in depressed excitability of pulpal A-fibers.

            The excitability of C-fibers is less affected than that of

            A-fibers by reduction in blood flow.



     v.     Presence of lymphatics in the dental pulp is a subject of

            controversary.



NERVE SUPPLYING PULP OF PRIMARY TEETH:

In maxillary primary teeth the pulp is supplied by

-    Maxillary central incisor

-    Maxillary lateral incisor     Anterior superior alveolar nerve

-    Maxillary canine

-    Maxillary first molar         Middle superior alveolar nerve

-    Maxillary second molar        Posterior middle superior alveolar
                                   nerve plexus

     In mandibular primary teeth pulp is supplied by mandibular

nerve. The mental nerve anesthetizes all mandibular teeth in the

quadrant.



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CAUSES OF PULP DISEASE (GROSSMAN ET AL., 1988)

I.    Physical

      A.   Mechanical

           1.    Trauma

                 a.     Accidental or sports injury

                 b.     Iatrogenic dental procedures (cavity or crown

                        preparation).

                 c.     Pathologic wear (attrition, abrasion)

                 d.     Crack tooth syndrome

                 e.     Barodontalgia

      B.   Thermal

                 a.     Heat from cavity preparation

                 b.     Exothermic heat from setting of cements

                 c.     Conduction of heat and cold through deep

                        fillings without a protective base.

                 d.     Frictional heat by polishing a restoration

      C.   Electrical

                 a.     Galvanic

                 b.     Currents

II.   Chemical

      A.   Phosphoric acid , acrylic monomer

      B.   Erosion (acids)




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III.   Bacterial

       A.      Toxins associated with caries

       B.      Direct invasion of pulp from caries or trauma

       C.      Microbial colonization in the pulp by blood borne

               microorganism (anachoresis)



DIAGNOSIS OF PULP PATHOLOGY

       Diagnosis is based upon a thorough information regarding

history of signs and symptoms.



I.     History of pain:

       Children are not good historians. Their symptoms are often

misleading because of their apprehension and parent involvement.

Therefore a detailed history of pain should be evaluated with very

simple questions of –

-      Is there any discomfort on eating sweet?

-      Is there any discomfort on eating ice-cream or drinking hot

       milk?

-      Is there any pain in the tooth at night while lying on the bed?

-      How long does the pain last?

-      How often do you get this pain?

-      Does your tooth jump when hit by toothbrush or spoon?




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     The presenting symptom while suggestive cannot be used

along to make the final diagnosis-

-    Pain-free: Presence or absence of pain is a very subjective

     symptom especially in children.

-    Sharp pain: Sharp pain due to external stimulus like cold

     which    gets    relieved    after     the   stimulus     is   removed   is

     associated      with   the    pulpodentinal        myelinated      A-delta

     neurofibers and the pulp is likely to be reversibly inflamed.

-    Severe pain which lingers: Is most often acute exacerbation of

     a chronic lesion and may be indicative of severe inflammation

     and is associated with C fibers.

-    Pain to hot relived b cold: Is also indication of severe

     inflammation.

-    Pain on biting: It suggests of a vital pulp with some necrosis

     within the pulp and an irreversible pulpitis of the vital tissue.



     Dental   pain    inflicted   by      deep    carious    lesion   has   been

classified as (Brahan and Morris, 1990).

-    Momentary pain

-    Persistent pain

-    Spontaneous pain




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     Momentary pain is that catalyzed by variation in temperature

or pH. Such stimuli evoke direct yet transient response eg., lost

restoration presenting exposed dentin or a carious lesion close to

pulp. In such cases, pulp is considered vital and in a reversible

state of inflammation. Inflammation is limited to coronal pulp in

737 of cases so pulpotomy has high degree of success.



     Persistent pain, continues even after the removal of the

stimulus and is indicative of inflammation extending into the pulp

canals. Pulpectomy is the choice of treatment.


     Spontaneous pain is the pain in the absence of a stimulus. It

also denoted inflammation of the pulp in the root canals. In

addition microscopic internal resorption is evident in the root

canals.


     According to Pinkham (1999) pain can be either „provoked‟ or

„spontaneous‟. Provoked pain is pain due to a stimulus and pulp is

in a reversible state. In spontaneous pain, pain is throbbing type

and it indicates advanced pulpal damage.



     Pain on lying down is also indicative of irreversible damage of

pulp and pain is due to increased intrapulpal pressure.




                                26
II.    Clinical observation:

       A careful extraoral and intraoral examination can be extreme

importance in detecting the presence of a pulpally involved tooth.


       Few clinical indications of pulp involvement are (Pinkham,

2001; Bessner and Ferrigno, 1989)

-      Redness and swelling of the vestibulum

-      Grossly decayed teeth with draining pus.

-      Missing or fractured restorations

-      Carious marginal breakdown

-      Extraoral swelling

-      Lymphnode involvement

-      Intraoral swelling

-      Fistula

-      Tooth discoloration

-      Traumatic injuries

-      Very deep carious lesion


III.   Diagnostic tools (Tandon, 2001; Pinkham, 2001)

-      Conventional methods

-      Newer techniques


Various conventional methods used are;

a.     Palpation:    Fluctuation    felt       by   palpating        a        swollen

       mucobuccal    fold    may   be    the    expression      of       an    acute

                                    27
     dentoalveolar abscess prior to exteriozation. Palpation is used

     to detect inflammation in the mucoperiosteum around the

     root of the tooth.


     Procedure: The index finger is pressed against the bone

     through the mucosa when pressure is felt, the finger is rolled

     causing sensitivity if inflammation is present. The result

     obtained should be compared to a contralateral tooth.

     Diagnostic information: A positive response is a indicator of

     periapical inflammation. However, if a positive response is not

     elicited inflammation is not necessarily absent.


b.   Mobility: Comparing the mobility of a suspicious tooth with

     its contralateral tooth is of particular importance. If a

     significant difference is observed pulpal inflammation might

     be suspected. But care must be taken not to misinterpret

     pathologic mobility with physiologic resorption.


c.   Percussion: Sensitivity to percussion may reveal a painful

     tooth in which inflammation has progressed to involve the

     periodontal ligament (acute apical periodontitis).


           Belanger (1988) suggests that percussion should be

     done gently with the tip of a finger and not with the end of a

     dental mirror to prevent exposing the child to unnecessary


                                 28
     uncomfortable stimuli constricted pupils are indicative of

     pain.


d.   Vitality tests: Such as sensitivity to heat or cold or electric

     pulp testing are of little value in children because false

     positive results may be obtained from stimulation of the

     gingival or of periodontal ligament. Also, because a child

     might be apprehensive, use of this type of stimulation by the

     dentist might lose the child‟s confidence causing disruptive

     behaviour.



             Pulp vitality is a function of vascular health, a vital

     pulp with an intact vasculature may test non-vital if only its

     neural component is injured as in recently traumatized teeth.

     For electric and thermal testing to be effective, the pulp must

     have sufficient member of mature neurons. However, both in

     primary and permanent teeth full alpha myelinated axon

     innervation is not present till 4-5 years after eruption. This

     reduced     number    of   pain   receptors   makes   them   less

     responsive to stimuli. Considering all these limitations these

     tests are not reliable in children.


e.   Radiographic examination: Inter-radicular radiolucencies a

     common finding in primary teeth with pulpal pathoses can be


                                  29
         better observed in bitewing radiographs or and IOPA x-ray.

         The integrity of the lamina dura of the affected tooth should

         be compared with that of adjacent teeth.


         Radiographs are valuable as aids in visualizing the presence

or absence of the following.

          Dental caries with possible or definite pulp involvement.

          Deep restorations close to a pulp horn.

          Successful or failing pulpotomy or pulpectomy.

          Pulpal changes, such as pulp calcification and pulp

           obliteration.

          Pathologic      root   resorptions   that   may    be    external   or

           internal. Internal root resorption indicates inflammation of

           a vital pulp whereas external root resorption demonstrate

           non-vital    pulp.     Physiologic    resorption    is    a   normal

           phenomenon of the primary dentition.

          Periapical and interradicular radiolucencies in primary

           teeth, any radiolucency associated with a non-vital tooth is

           located in furcation area because of the presence of

           accessory canal in the pulpal floor and decrease trunk

           width of the root.


f.       Operative diagnosis: Depending upon time and colour of

         bleeding to know extent of inflammation.


                                        30
Newer methods:

a.   Laser Doppler Flowmetry:

     It   is   a    noninvasive,   objective,     painless   alternative   and

therefore a promising test for young children. It was first developed

in the 1970‟s to measure the velocity of red blood cells in

capillaries. The flowmeter produced regular signal fluctuations for

vital teeth. Non-vital teeth showed no such synchronous signal but

produced irregular fluctuations or very steep spike traces that were

attributed     to    a   movement     artifact.     This     instrument    has

demonstrated its value for ongoing assessment of post-traumatized

permanent incisors.



b.   Pulp oximetry in evaluation of vitality:

     A direct measurement of pulp circulation is the only real

measure of pulp vitality. Pulp oximetry is a completely objective

test, requiring no subjective response from the patient, that

directly measures blood oxygen saturation levels.



     To determine oxygen saturation, pulse oximeter measures and

compares amplitudes of the ratios of transmitted infra red with red

light. This ratio varies with relative fractions of oxygen saturated to

unsaturated haemoglobin and used to calculate oxygen saturation.

These characteristics infer that pulse oximeter is also capable of


                                     31
evaluating    the   blood   vasculature     status   within   a   tooth    and

therefore pulp vitality.



        The dependence on a pulsative blood flow appears to be a

disadvantage of the use of the pulse oximeter.



c.      Dual wavelength spectrometry :
        This measures blood oxygenation change within the capillary

bed of dental tissue and thus not dependent on pulsatile blood

flow.



d.      Hughes probe camera:

        This is used in detecting temperature change as small as

0.1 0 C hence measuring pulp vitality experimentally.



Clinical considerations:

Effect of local anaesthesia on the pulp (Cohen and Burn, 1997)

        Addition of a vasoconstriction to a local anesthetic is to

potentiate and prolong the anesthetic effect by reducing the blood

flow in the area. However, it is advisable to use vasoconstrictor free

LA for restorative procedures for vital. However dental treatments

where vitality of the pulp is not of concern eg., endodontic therapy

or   extractions,   the     use   of   vasoconstrictor   containing       local

anesthetic is recommended.

                                       32
        Both infiltration and mandibular block injection cause a

significant decrease in pulpal blood flow.                  There is a direct

relationship between the length of the flow cessation and the

concentration       of   vasoconstrictor     used     pulpal   blood   flow   and

sensory nerve activity return to normal levels after 3 hours of total

cessation of blood flow. Irreversible pulpal injury is apt to occur if

procedures like full crown preparation is performed immediately as

is caused by release of substantial amount of vasoactive P

substance into the extracellular compartment of the underlying

pulp which cannot be removed quickly because of decreased blood

flow.


        Increased    tissue      pressure    occurs    in   response    to    pulp

inflammation. In acute inflammation chemical mediators released

from injured cells excite sensory nerve fibers, which then act on the

muscular elements of the blood vessels and cause dilation of

vessels, also the increased permeability of the vessels permits the

escape of plasma proteins and leucocytes from the capillaries into

the     inflamed    area    to    carryout    neutralization,    dilution     and

phagocytosis of the irritant. Thus during inflammation the effects

of infiltration anesthesia are diluted which results in diminution of

anesthesia (Seltzer and Bender, 2000).




                                        33
      Once the anesthetic solution is deposited in the tissues, the

extracellular fluid that surrounds the cells immediately begins to

dilute it. The molecules of the solution diffuse in all direct ions with

the concentration diminishing in geometric ratio as it leaves the

original area of deposition. Thus greater the distance of the original

injection from target area, fewer themolecules that reach the

desired site and lower the intensity of the resulting block.



      Arrangement of nerve fibers in bundles often contributes to

„spotty‟ anesthesia. As a result mantle fibers which innervate

proximal structures (usually soft tissues) may be blocked, while the

distally innervating (usually hard tissues) core fibers may be

unaffected, which explains why occasionally inferior alveolar nerve

block symptoms are present although still pain persists in the

tooth.



      An anesthetic solution injected into a highly vascular area is

rapidly   absorbed   into   the   systemic   circulation.   This   rapid

absorption soon reduces the effective concentration outside the

nerve and causes a more rapid termination of satisfactory analgesia

(Bennett, 1990).




                                   34
CONCLUSION:

       A comprehensive knowledge of the dental pulp is essential to

know    the   mechanism   of   various   pulpal   pathologies   and   a

comprehensive knowledge of pulpal pathologies help in diagnosing

correctly these clinical entities. A correct diagnosis will thus help

in proper planning of the treatment to be rendered, all thereby

aiding in establishing a healthy dentition.




                                  35
REFERENCES:

Belanger G.K. (1988): “Pulp therapy for the primary dentition”. In

     Pinkham Jr.: Pediatric dentistry infancy through adolescence.

     Philadelphia, W.B. Saunders Co.

Bennett, C.R.: “Local anesthesia and anesthetic solution”. In

     Monheim‟s    local    anesthesia    and   pain   control   in   dental

     practice, 7 th Ed., 1990: 134-135.

Brannstrom M. and Garberoglio R. (1972): “The dentinal tubules

     and the odontoblast processes”. Acta. Odontol. Scand.30:291.

Cohen, S. and R.C. Burn: “Pulp development, structure and

     function”. In pathways of pulp, 1997: 296-336.

England   M.C.,   Pellis    E.G.   and    Michanowicz      A.E.      (1974):

     “Histopathologic study of the effect of pulpal disease upon

     nerve fibers of the human dental pulp”. Oral Surg. 38: 783.

Farnoush A. (1984): “Mast cells in human dental pulp”. J. Endod.

     10: 250.

Fearnhead R.W. (1961): “The neurohistology of human dentine”.

     Proc. Roy Soc. Med. 54: 877.

Fitzgerald M., Chiego D.J. and Heys D.R. (1990): “Autoradiographic

     analysis of odontoblast replacement following pulp exposure

     in primate teeth”. Arch Oral Biol. 35: 707.

Fuss Z. et al. (1986): “Assessment of reliability of electrical and

     thermal pulp testing agents”. J. Endod. 12: 301.


                                   36
Grossman L.J., Oliet S. and Rio C.E.D. (1988): “Disease of dental

     pulp in endodontic practice”. 11 th Ed.: 59-60.

Hahn C.L., Falkler W.A. Jr and Siegel M.A. (1989): “A study of T

     cells and B cells in pulpal pathosis”. J. Endod. 15: 20.

Harris R. and Griffin C.J. (1968): “Fine structure of nerve endings

     in the human dental pulp”. Arch Oral Biol. 13: 773.

Holland G.R. (1975): “Membrane junctions on car odontoblasts”.

     Arch Oral Biol. 20: 551.

Holland    G.R.   (1976):   “Lanthanum      hydroxide     labeling   of   gap

     junctions in the odontoblast layer”. Anat. Rec. 186: 121.

Holland G.R. (1976): “The extent of the odontoblast process in the

     cat”. J. Anat. 121: 133.

Holland G.R. (1985): “The odontoblast process: form and function”.

     J. Dent. Res. 64: 499.

Kim S. et al. (1982): “Effects of bradykinin on pulpal blood flow in

     dogs”. J. Dent. Res. 61: 293.

Koling    A.   (1988):    “Structural    relationships    in   the   human

     odontoblast layer, as demonstrated by freeze fracture electron

     microscopy”. J. Endod. 14: 239.

Pinkham (2001): “Pulp therapy for the primary dentition”. In

     Pinkham       Jr.:     Pediatric    dentistry:      Infancy     through

     adolescence. 3 rd Ed.: 341-356.




                                    37
Reader A. and Foreman D.W. (1981): “An ultrastructural qualitative

     investigation of human intradental innervation”. J. Endod. 7:

     161.

Seltzer, S. and J.B. Bender: “The circulation of the pulp”. In

     Seltzer‟s the dental pulp, 3 rd Ed., 2000: 105-130.

Sigal M.J. et al. (1984): “A combined scanning electron microscopy

     and    immunofluorescence      study    demonstrating       that   the

     odontoblast process extends to the dentinoenamel junction in

     human teeth”. Anat. Red. 210: 453.

Sigal M.J. et al. (1984): “The odontoblast process extends to the

     dentinoenamel junction: An immunocytochemical study of rat

     dentine”. J. Histochem. Cytochem. 32: 872.

Smulson M.H. and Sieraslas S.M. (1996): “Histophysiology and

     diseases of the dental pulp in endodontic therapy”. Weine

     F.S. ed. 5 th Ed.: 84-165.

Tendon (2001): “Pediatric endodontics in textbook of pedodontics”.

     1 st Ed.: 328-334.

Thomas H.F. (1979): “The extent of the odontoblast process in

     human dentin”. J. Dent. Res. 58: 2207.

Torebjork   H.E.   and    Hanin   R.G.   (1973):   “Perceptual    changes

     accompanying controlled preferential blocking of A and C

     fiber responses in intact human skin nerves”. Exp. Brain Res.

     16: 321.


                                   38
Torneck C.D.: “Dentin-pulp complex”. In Ten Cate A.R.: Oral

     histology: development, structure, and function. 2 nd Ed.,

     Louis, 1985, Times Mirror/Mosby College Publishing.

Trowbrdge H.O. and Kim S. (1997): “Pulp development, structure

     and function in pathways of the pulp”. Cohens R.C., Burn Ed.

     6 th Ed.: 296-336.




                               39
                          DENTAL PULP


                             CONTENTS


       Introduction

       Definitions of dental pulp

       Functions of dental pulp

       Development of dental pulp

       Anatomic structure of dental pulp

       Morphologic zones of dental pulp

       Structural elements of dental pulp

            Cellular
            Extracellular
       Nerve supply of pulp in primary dentition

       Causes of pulpal diseases

       Summary of inflammatory activity

       Pulpal pathophysiology

       Mechanism of pulp and periapical inflammatory response

       Classification of pulpal diseases

       Diagnosis of pulpal pathologies

            Conventional methods
            Newer methods
       Clinical considerations

       Conclusions

       References

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