Ch02: HISTOLOGY AND PHYSIOLOGY OF THE …...Histology and Physiology of the Dental Pulp 27 The human...

As the principal source of pain within the mouth andas the major site of attention in endodontic treatment,the pulp warrants direct inspection. By its very locationdeep within the tooth, it defies visualization, other thanits appearance as radiolucent lines on radiographs.Occasionally, when required to deal with an accidental-ly fractured cusp, the dentist is afforded a glimpse ofthe normal pulp. A pink, coherent soft tissue is noted,obviously dependent on its normal hard dentin shellfor protection and hence, once exposed, extremely sen-sitive to contact and to temperature changes.

When pulp tissue is removed en masse from a toothin the course of, say, vital pulpectomy, the dentist gainsa new perspective of the pulp. Here is connective tissueobviously rich in fluid and highly vascular. After expo-sure to air, the appearance and volume of the tissuechange as the fluid evaporates. Another dimension ofthe physical characteristics of pulp tissue can be demon-strated by grasping a freshly extirpated vital pulpbetween thumb and forefinger in both hands andattempting to pull the pulp apart. Surprisingly, this tinystrand has much the feel of dental floss: it is tough,fibrous, and inelastic. This is a reflection of an impor-tant structural component of the pulp, namely collagen.

FUNCTION

The pulp lives for the dentin and the dentin lives by thegrace of the pulp. Few marriages in nature are markedby a greater interrelationship. Thus it is with the pulpand the four functions that it serves: namely, the for-mation and the nutrition of dentin and the innervationand defense of the tooth.1

Formation of the dentin is the primary task of thepulp in both sequence and importance. From the meso-dermal aggregation known as the dental papilla arises thespecialized cell layer of odontoblasts adjacent and inter-nal to the inner layer of the ectodermal enamel organ.Ectoderm interacts with mesoderm, and the odonto-

blasts initiate the process of dentin formation.2 Onceunder way, dentin production continues rapidly until themain form of the tooth crown and root is created. Thenthe process slows, eventually to a complete halt.

Nutrition of the dentin is a function of the odonto-blast cells and the underlying blood vessels. Nutrientsexchange across the capillaries into the pulp interstitialfluid, which, in turn, travels into the dentin through thenetwork of tubules created by the odontoblasts to con-tain their processes.

Innervation of the pulp and dentin is linked by thefluid and by its movement between the dentinal tubulesand peripheral receptors, and thus to the sensorynerves of the pulp proper.3

Defense of the tooth and the pulp itself has beenspeculated to occur by the creation of new dentin in theface of irritants. The pulp may provide this defense byintent or by accident; the fact is that formation of lay-ers of dentin may indeed decrease ingress of irritants ormay prevent or delay carious penetration. The pulpgalvanizes odontoblasts into action or produces newodontoblasts to form needed hard tissue.

The defense of the pulp has several characteristics.First, dentin formation is localized. Dentin is produced ata rate faster than that seen at sites of nonstimulated pri-mary or secondary dentin formation. Microscopically,this dentin is often different from secondary dentin andhas earned several designations: irritation dentin, repara-tive dentin, irregular secondary dentin, osteodentin, andtertiary dentin.

The type and amount of dentin created during thedefensive response appear to depend on numerous fac-tors. How damaging is the assault? Is it chemical, ther-

Chapter 2

HISTOLOGY AND PHYSIOLOGY OF THE DENTAL PULP

David H. Pashley, Richard E. Walton, and Harold C. Slavkin

*Supported, in part, by grant DE 06427 from the NationalInstitute of Dental and Craniofacial Research.

mal, or bacterial? How long has the irritant beenapplied? How deep was the lesion? How much surfacearea was involved? What is the status of the pulp at thetime of response? A second defensive reaction, inflam-mation within the pulp at the site of injury, should notbe ignored. This phenomenon will be explored in moredetail in chapter 4.

INDUCTION AND DEVELOPMENT OF DENTIN AND CEMENTUM

Human tooth development spans an extremely longperiod of time, starting with the induction of the pri-mary dentition during the second month of embryoge-nesis until completion of the permanent dentitiontoward the end of adolescence. The primary dentitionis induced during the fifth week of gestation, and bio-mineralization begins during the fourteenth week ofgestation. In tandem, the first permanent teeth havereached the bud stage, and they begin biomineraliza-tion just prior to birth. The first primary teeth begin toerupt in children at 6 months of age, and the first per-manent teeth erupt at 5 to 6 years of age. The thirdmolars are the last teeth to be formed, and their crowndevelopment is completed between 12 and 16 years ofage. Therefore, the induction and development of thehuman dentition persists during embryonic, fetal,neonatal, and postnatal childhood stages of develop-ment. Detailed descriptions of the histology and timingof human tooth development can be readily found in anumber of excellent textbooks.4

Inductive tissue interactions, specifically epitheli-um-mesenchyme interactions, have been extensivelyinvestigated and characterized throughout the variousstages of tooth crown and root morphogenesis.5–8 Thedeveloping tooth system has become a well-character-ized model for defining the molecular mechanismsrequired for reciprocal signaling during epithelium-mesenchyme interactions in crown and root morpho-genesis and cytodifferentiation.9–13

It is now evident that the initial inductive signals fortooth formation are synthesized and secreted from spe-cific sites defined as odontogenic placodes within theoral ectoderm that cover the maxillary and mandibularprocesses.13 The oral ectodermally derived inductivesignals are received by multiple cognate receptors locat-ed on the cell surfaces of a specific subpopulation ofcranial neural crest–derived ectomesenchymal cellsduring the initial induction process and the subsequentdental lamina, bud, and stages of tooth develop-ment8–13 (Figure 2-1).

During the transition from bud to cap stages, theectomesenchyme provides several cell lineages, including

26 Endodontics

one that becomes dental papilla mesenchyme and othersthat become progenitor cells for the subsequent devel-opment of the periodontium.8,14,15 At this time, multipleand reciprocal signals are secreted by the dental papillamesenchyme, and these signals bind to the extracellularmatrix and transmembrane cell receptors along the adja-cent enamel organ epithelium. A discrete structure with-in the enamel organ, termed the “enamel knot,” synthe-sizes and secretes a number of additional signals thatalso participate in the determination for the patterns ofmorphogenesis within the maxillary and mandibulardentitions: incisiform, caninform, and molariform.12,13

Figure 2-1 Early dental pulp, or dental papilla, exhibiting a cellu-lar mass at the center of this tooth bud in the early bell stage. Nervefiber bundles are evident in cross-section as dark bodies apical todental papilla yet are absent in the papilla itself. Human fetus, 19weeks. Palmgren nerve stain. Reproduced with permission fromArwil T, Häggströms I. Innervation of the teeth. Transactions RoyalSchool of Dentistry (Stockholm), 3:1958.

Histology and Physiology of the Dental Pulp 27

The human genome was basically completed by theyear 200016; essentially all of the 100,000 regulatoryand structural genes within the human lexicon havebeen identified, sequenced, and mapped to specificchromosomal locations. Further, combinations ofgenes encoded within the human genomic deoxyri-bonucleic acid (DNA) are now known to be expressedduring development that controls morphogenesis. Anumber of these genes have been identified and char-acterized as being expressed in the odontogenic pla-code, dental lamina, and the bud, cap, bell, and crownstages of tooth development in either the epithelial ormesenchymal cells or both. Significantly, these genesare expressed in various combinations during induc-tion processes associated with many developing epider-mal organ systems including the salivary gland, seba-ceous glands, mammary glands, tooth, hair, and skinmorphogenesis.5

The specificity of induction reflects the particularcombinations of signaling molecules, their cognate cellsurface receptors, various intracellular signal pathways,and a large number of transcriptional factors that reg-ulate gene expression. These combinations further aremodified according to temporal and spatial informa-tion during development; the combination used toinduce the dental lamina is different than that required

for cap stage development and subsequent odontoblastcytodifferentiation. The hierarchy of these molecularmechanisms associated with the initiation and subse-quent early stages of tooth development is shown inFigure 2-2.

Specific mutations or alternations in one or more ofthese molecules result in clinical phenotypes includingcleft lip and/or palate and a range of dental abnormali-ties with enamel, dentin, cementum, periodontal liga-ment, or alveolar bone disorders; for example,hypodontia or missing teeth as seen in X-linked anhy-drotic ectodermal dysplasia, which is caused by a muta-tion in the gene EDA; familial tooth agenesis, which iscaused by a mutation in the gene MSX1; and X-linkedamelogenesis imperfecta, which is caused by a mutationin the gene amelogenin.17,18 Recently, a mutation in thegene CBF-alpha1, a transcription factor, was found tocause cleidocranial dysplasia with hyperdontia.19

The development of dentin is intriguing for severalreasons. First, signals within the inner enamel epitheliaof the enamel organ induce adjacent cranial neuralcrest–derived ectomesenchymal cells to become pro-genitor odontoblasts. Mutations in either the signalingmolecules, cognate receptors, intracellular signal path-ways, transcription factors, or extracellular matrix mol-ecules can result in severe dental anomalies including

Figure 2-2 Molecular controls for the initiation and early stages of tooth morphogenesis. The initiation or site selection for tooth develop-ment is controlled by oral ectoderm-derived epithelial fibroblast growth factor (FGF) and bone morphogenetic protein (BMP) through theirsignaling pathways. The actions of these signaling pathways or circuits are dependent on the stage and position of development and the com-bination of transcription factors that are either induced (→) or repressed (_). This establishes the odontogenic placode. Thereafter, epithe-lium regulates the adjacent mesenchyme during the bud stage and the mesenchyme then promotes differentiation and influences the adja-cent inner enamel epithelium through feedback loops in the cap, bell, and crown stages of tooth development. The reader is encouraged tosee the following references for detailed analyses of these morphoregulatory molecules.2,7–10,14,16

tooth agenesis, hypodontia, and oligodontia and defectsin dentin deposition or biomineralization, termeddentinogenesis imperfecta. Several dentin extracellularmatrix proteins—dentin sialoprotein, dentin matrixprotein, and dentin phosphoprotein—are produced byalternative splicing from one single gene product.Mutations in any one of these encoded sequences, or intype I collagen, result in dentinogenesis imperfecta.Mutations that are limited to type I collagen produceosteogenesis imperfecta with a form of dentinogenesisimperfecta.

Following crown morphogenesis, cells from the cer-vical loop give rise to Hertwig’s epithelial root sheath(HERS) cells, which, in turn, induce adjacent dentalpapilla mesenchymal cells to engage in root forma-tion.6–8 Progressive cell proliferation and migrationseventually outline the shape and size of the formingroots. In this developmental process, two interpreta-tions are currently being considered. First, evidence isavailable to support the hypothesis that HERS cellstransdifferentiate into cementoblasts and secrete acel-lular cementum matrix.8 Second, evidence is also avail-able to support the hypothesis that peripheral ectomes-enchymal cells penetrate through the HERS andbecome cementoblasts and secrete acellular cemen-tum.6,7 Of course, both processes may take place at dif-ferent times and positions of cementogenesis.

The understanding of the induction and develop-ment of cementum has also progressed in recent years.Hertwig’s epithelial root sheath cells provide signalsthat induce the differentiation of odontoblasts and theformation of the first peripheral layer of dentin. It hasbeen known for almost 100 years that a small percent-age of the human population expresses enamel pearlsalong the root surfaces of permanent teeth. Theseenamel-like aberrations in cementogenesis are intrigu-ing and could offer new insights and strategies toregenerate acellular cementum.

Recent advances have indicated that molecules pre-sumed to be uniquely restricted to inner enamelepithelium and ameloblasts associated with enamelformation are also expressed in HERS.6–8 Specifically,ameloblastin has recently been identified in bothameloblasts and HERS.20 This association betweenenamel and cementum has been previously discussedwith respect to coronal cementum.21 These and otherstudies have suggested that enamel matrix containsmolecular constitutents, presumably with growth fac-tor bioactivities, that can induce acellular regenerationwhen active on denuded human dentin root surfaces.Recently, an enamel matrix preparation has beendemonstrated to induce acellular cementum regenera-

28 Endodontics

tion on root surfaces associated with advanced peri-odontitis.22 The available evidence strongly supportsthe hypothesis that enamel organ epithelium-derivedcell phenotypes control coronal enamel deposition andthe initiation of acellular cementum formation.23,24

ANATOMY

The living pulp, as we have seen, creates and shapes itsown locale in the center of the tooth. The pulp, undernormal conditions, tends to form dentin evenly, faci-olingually and mesiodistally.25 The pulp therefore tendsto lie in the center of the tooth and shapes itself to aminiaturization of the tooth. This residence of the pulpis called the pulp cavity, and one speaks of its two mainparts as the pulp chamber and the root canal. The clin-ical implications of pulp form and variation are exten-sively covered in chapter 10. Indeed, the key word inunderstanding the gross anatomy of the pulp is “varia-tion.” Equally evident in any study of the pulp is thereduction in size of the chamber and canals with age.Such reduction in size thus becomes a new variation.

In addition to changes in pulp size and shape withaging, external stimuli also exert an effect. Caries, attri-tion, abrasion, erosion, impact trauma, and clinicalprocedures are some of the major irritants that maycause formation of irritation dentin. The clinicianmust appreciate the resultant alterations in internalanatomy that accompany disease and damage of thepulp and dentin.

Pulp Chamber

At the time of eruption, the pulp chamber of a toothreflects the external form of the enamel.1 Anatomy isless sharply defined, but the cusp form is present. Oftenthe pulp suggests its original perimeter (and threatensits future) by leaving a filament of itself, the pulp horn,within the coronal dentin. A specific stimulus such ascaries leads to the formation of irritation dentin on theroof or wall of the chamber adjacent to the stimulus. Ofcourse, with time, the chamber undergoes steadyreduction in size as secondary, and irritation dentin isproduced on all surfaces (Figure 2-3).

Root Canal

An unbroken train of connective tissue passes from theperiodontal ligament through the apical root canal(s) tothe pulp chamber. Each root is served by at least one suchpulp corridor. Actually, the root canal is subject to thesame pulp-induced changes as the chamber. Its diameterbecomes narrowed, rapidly at first as the foramen takesshape in the posteruptive months but with increasingslowness once the apex is defined. The canal diameter


tends to decrease slightly with age; irritants such as peri-odontal disease may cause further constriction.

According to Orban, the shape of the canal,“to a largedegree, conforms to the shape of the root. A few canalsare round and tapering, but many are elliptical, broadand thin.”26 A curve at the end of the root means almostinvariably that the canal follows this curve. Meyer statedthat “roots that are round and cone-shaped usually con-tain only one canal, but roots that are elliptical and haveflat or concave surfaces more frequently have morecanals than one”27 (Figure 2-4).

The foramen can change in shape and locationbecause of functional influences on the tooth28 (eg,tongue pressure, occlusal pressure, mesial drift). Thepattern that develops is the reverse of the changes in thealveolar bone around the tooth. Cementum resorptionoccurs on the wall of the foramen farthest from theforce and apposition on the wall nearest. The net resultis a deviation of the foramen away from the true apex(Figure 2-5).

Figure 2-3 Schematic diagram of a mandibular molar showinghard tissue apposition with time and/or irritation. Black arrowsindicate physiologic secondary cementum and dentin apposition;white arrows indicate formation of dentin in response to irritants.Pulp space undergoes continual reduction in size and volume. Notethat the floor of the chamber is a region of maximum secondarydentin formation.

Figure 2-4 Canal size and shape are a reflection of the externalroot surface. The upper diagrams show the possible canal config-urations within each shaped root. The maxillary molar root sec-tions illustrate that all sizes and shapes of canals may be seen in asingle tooth.

Figure 2-5 Features often noted in normal yet aging tooth: devia-tion of apical foramen as a result of mesial migration of the tooth(top arrow). Selective resorption and apposition of cementum havechanged the position of the apex, causing narrowing of the apicalthird of the root canal by increments of secondary dentin and flar-ing of apical foramen from its smallest diameter at the dentinoce-mental junction (bottom arrow) to its greatest diameter at thecemental surface. Note the abundance of collagen fibers in theradicular pulp. Reproduced with permission from Matsumiya S.Atlas of oral pathology. Tokyo Dental College Press; 1955.

Foramina

The anatomy of the root apex is partially determinedby the number and location of apical blood vesselspresent at the time of formation of the apex. When thetooth is young and just erupting, the foramen is open.Islands of dentin may appear within the mainstream ofconnective tissue when the root sheath has inducedthem, but these islands are widely separated.Progressively, the main channel narrows. The primaryvessels and nerves, though never directly threatenedwith strangulation, have a restricted passage.Increments of cementum apposition contribute to thiscontinuous modeling. The possibilities of vascularbranching are so varied at the apex that prediction ofthe number of foramina in a given tooth becomesimpossible (Figure 2-6).

It is known that the incidence of multiple foraminais high.29,30 The majority of single-rooted teeth have asingle canal that terminates in a single foramen. Lessoften, they possess an apical delta, which terminates ina major channel and one or more collateral exits.Occasionally, the delta has several channels of equalmagnitude. Root canals of the multirooted teeth, onthe other hand, tend to have a more complex apicalanatomy. Multiple foramina are the rule rather than theexception. When accessory foramina are found in oneroot of a multirooted tooth, the other roots usually

30 Endodontics

have a similar condition.29 Moreover, because the indi-vidual roots of such teeth often contain two or eventhree canals, a new factor is introduced. These canalscan merge, but they need not and often do not mergebefore making their exit. Indeed, each may leave theroot independently. Branching of the emergent canalswithin the apical area is a common finding because thepreexisting vessels are linked.30

It is also important to recall that cementum forms inabundance at the root apex. Because of the appositionof new layers of cementum, in response to eruption, theforamen anatomy is by no means constant. As statedabove, the center of the foramen tends to deviateincreasingly from the apical center.31 Also, many rootcanals have two apical diameters. The minor diameterat the level of the dentinocemental junction can be assmall as one half that of the major diameter at theexternal surface of the root. Cementum depositiontends to produce an apical funnel of increasing diver-gence. Contributing to this is secondary dentin forma-tion that narrows the dentinal orifices of the canal (seeFigure 2-5).

Stereomicroscopic analysis of some 700 posteriorroot apices showed that at least half of the majorforamina take eccentric positions that deviate as far as2 mm from the apex.29Accessory foramina, on average,were found to be located twice the distance of themajor foramina from the vertex (Figure 2-7).29

Accessory Canals

Communication of pulp and periodontal ligament is notlimited to the apical region. Accessory canals are foundat every level. Vascular perfusion studies have demon-strated vividly how numerous and persistent these trib-utaries are.32 Many, in time, become sealed off bycementum and/or dentin; however, many remain viable.The majority appear to be encountered in the apical halfof the root. These generally pass directly from the rootcanal to the periodontal ligament (Figure 2-8).

A common area in which accessory canals appear isthe furcation area of molar teeth (Figure 2-9). Burchand Hulen33 and Vertucci and Anthony34 found thatmolars frequently presented openings in the furcationareas. However, the studies did not determine howmany of these represented patent (continuous) acces-sory canals all the way from the pulp to the periodon-tal ligament. Morphologic and scanning electronmicroscopic studies consistently show the presence ofpatent accessory canals or depressions that wereassumed to be the openings to such canals.34–37 Inother studies, dyes were injected or drawn by vacuuminto the furcation of molars. Approximately one half of

Figure 2-6 Diverse ramifications of apical pulp space anatomy.These models were made by drawing pulps from serial histologicsections and “stacking” the drawings. Many regions are obviouslyinaccessible to conventional débridement methods. Adapted withpermission from Meyer W. Dtsch Zahnaerztl Z 1970;25:1064.


the teeth studied demonstrate patent accessory canalsfrom pulp space to furcation.38

HISTOLOGY

Regions

Classically, the pulp is described as having two definedregions, central and peripheral.39 Typically, however,studying sections of pulp under the microscope revealsthat the classic description is not consistent; levels ofactivity dictate regional morphology. However, it ishelpful to know the textbook description before study-ing the variations.

The pulp is in intimate contact with the dentin andsurvives only through the protection of its hard outercovering. As the price of this protection, the pulp con-

tributes to a close symbiosis. The way in which the nor-mal pulp relates to its immediate environment can bebest explained by a review of its own morphology andthat of the tissues with which it is confluent, namely, thedentin and the periodontal ligament. In general, the pulpdemonstrates a homogeneity in its blend of cells, inter-cellular substance, fiber elements, vessels, and nerves.

Peripheral Pulp Zone. On the periphery of thepulp, adjacent to the calcified dentin, structural layersare apparent. These are usually evident in amedium-power photomicrograph (Figure 2-10). Nextto the predentin lies the palisade of columnar odonto-blast cells. Central to the odontoblasts is the subodon-toblastic layer, termed the cell-free zone of Weil.40

Figure 2-7 Accessory foramen (arrow) in mandibular anteriortooth. Accessory foramina are usually located within the apical 2 to3 mm of root. (Orban collection.) Reproduced with permissionfrom Sicher H. Oral histology and embryology. 5th ed. St. Louis: CVMosby; 1962.

Figure 2-8 A, Necrotic pulp in maxillary second premolar inwhich irritants egress through lateral canals to the periodontium,creating inflammatory lesions (arrows). Although often invisible onpretreatment radiographs, the presence of lateral canals may beconfirmed following obturation. B, Bony lesions healed severalmonths following root canal treatment. Accessory canals are impor-tant, not so much for the irritants they contain but because of theircommunication to the PDL. (Courtesy of Dr. Manuel I. Weisman.)

A

B

Plexuses of capillaries and small nerve fibers ramify inthis subodontoblastic layer. Deep to the odontoblasticlayer is the cell-rich zone, which blends in turn with thedominant stroma of the pulp. The cell-rich zone con-tains fibroblasts and undifferentiated cells, which sus-tain the population of odontoblasts by proliferationand differentiation.41

These zones vary in their prominence from tooth totooth and from area to area in the pulp of the sametooth. The cell-free and cell-rich zones are usuallyindistinct or absent in the embryonic pulp and usuallyappear when dentin formation is active. The zones tendto become increasingly prominent as the pulp ages.Both of these zones are less constant and less promi-nent near the root apex.

Central Pulp Zone. The main body of the pulpoccupies the area circumscribed by cell-rich zones. Itcontains the principal support system for the periph-eral pulp, which includes the large vessels and nerves(Figure 2-11) from which branches extend to supplythe critical outer pulp layers. The principal cells arefibroblasts; the principal extracellular components areground substance and collagen. The environment ofthe pulp is unique in that it is surrounded by anunyielding tissue and fed and drained by vessels thatpass in and out at a distant site. However, it is classi-fied as an areolar, fibrous connective tissue, contain-ing cellular and extracellular elements that are foundin other similar tissues. These elements will be dis-cussed in more detail.

32 Endodontics

Structural Elements, Cellular

Reserve Cells. The pulp contains a pool of reservecells, descendants of undifferentiated cells in the primi-tive dental papilla. These multipotential cells are likely afibroblast type that retains the capability of dedifferen-tiating and then redifferentiating on demand into manyof the mature cell types. Beneath the odontoblasts, inthe cell-rich zone, are concentrations of such cells.However, Frank demonstrated by radioautography thatthese cells produce little collagen, which is circumstan-tial evidence that they are not mature fibroblasts.42

Baume has reviewed ultrastructural studies that sug-gest cytoplasmic connections between the odontoblastsand these subjacent mesenchymal cells.43 Throughsuch connections, on odontoblast injury or death, sig-nals may be provided to these less differentiated cellsthat may cause them to divide and differentiate intoodontoblasts or odontoblast-like cells, as required.43

Also important are the reserve cells scatteredthroughout the pulp, usually in juxtaposition to bloodvessels. These retain the capacity, on stimulation, todivide and differentiate into other mature cell types.For example, mast cells and odontoclasts (tooth resor-bers) arise in the presence of inflammation.

Significant are the unique cells that differentiate toform the calcified tissue that develops under a pulp capor pulpotomy when calcium hydroxide is placed indirect contact with the pulp. These unique cells are alsofrequently observed along the calcified tissue formingat the base of tubules involved with caries, restorations,attrition, or abrasion. This calcified tissue is not a true

Figure 2-9 Inset demonstrates method of sectioning molars for viewing furcations. A, Foramina of accessory canal indicated by arrow (×20original magnification). B, Foramen seen in A, magnified ×1,000. Canal is about 35 microns across, flaring to 60 microns at surface. Notetwo peripheral foramina on the rim. Reproduced with permission from Koenigs JG, Brilliant JD, Foreman DW. Oral Surg 1974;38:773.

A B


Figure 2-10 A, Medium-power photomicrograph from human pulp specimen showing dentin (D), predentin (P), odontoblast layer (O),cell-free zone (CF), cell-rich zone (CR), and central pulp (CP). B, Region similar to area bracketed in A. Cell-free zone contains large num-bers of small nerves and capillaries not visible at this magnification. Underlying CR does not have high concentration of cells but containsmore cells than does central pulp. (A and B courtesy of Drs. Dennis Weber and Michael Gaynor.) C, Diagram of peripheral pulp and its prin-cipal elements. D, Scanning electron micrograph of dentin-pulp junction. Note corkscrew fibers between odontoblasts (arrow). Reproducedwith permission from Jean A, Kerebel JB, Kerebel LM. Oral Surg 1986;61:592. E, Scanning electron micrograph of pulpal surface of odonto-blast layer. Thread-like structures are probably terminal raveling of nerves. (Courtesy of Drs. R. White and M. Goldman.)

C

A B

D

E

dentin, just as the cells that produce it are not trueodontoblasts. However, like the odontoblast, these cellstrace their origins to undifferentiated cells.

Fibroblasts. Most of the cells of the pulp arefibroblasts. These cells exhibit wide variation in theirdegree of differentiation.44 Baume refers to them asmesenchymal cells, pulpoblasts, or pulpocytes in theirprogressive levels of maturation.43 These distinctionsare made, in part, because of the ability of these cells toform calcified tissues, something regular connective tis-sue fibroblasts apparently cannot accomplish.

Pulpal fibroblasts are spindle-shaped cells withovoid nuclei (Figure 2-12). They synthesize and secretethe bulk of the extracellular components, that is, colla-gen and ground substance. The classic autoradiograph-ic studies of Weinstock and Leblond, using 3H-proline,

34 Endodontics

demonstrated the process of collagen synthesis andsecretion by the fibroblast.45

Not only are fibroblasts the principal producers ofcollagen, they also eliminate excess collagen or partici-pate in collagen turnover in the pulp by resorption ofcollagen fibers. This has been demonstrated to occurintracellularly by the action of lysosomal enzymes,which literally digest the collagen components.46

Defense Cells.Histiocytes and Macrophages. Undifferentiated

mesenchymal cells (see Figure 2-12) around blood ves-sels (pericytes) can differentiate into fixed or wander-ing histiocytes under appropriate stimulation.47

Wandering histiocytes (macrophages) may also arisefrom monocytes that have migrated from vessels. Thesecells are highly phagocytic and can remove bacteria,foreign bodies (endodontic paste, zinc oxide, etc), deadcells, or other debris.48 Pulpal macrophages and den-dritic cells thought to function like Langerhans’ cellshave been identified in normal rat pulp.49 These cellsseem to be associated with pulpal immunosurveillance.

Polymorphonuclear Leukocytes. The most commonform of leukocyte in pulpal inflammation is the neu-trophil, although eosinophils and basophils are occa-sionally detected. It is important to know that althoughneutrophils are not normally present in intact healthypulps, with injury and cell death they rapidly migrateinto the areas from nearby capillaries and venules.50

They are the major cell type in microabscess formationand are very effective at destroying and phagocytizingbacteria or dead cells. Unfortunately, their participa-tion often injures adjacent cells and may contribute tothe development of wider zones of inflammation.

Figure 2-11 Cross-section from the central pulp showing majorsupport systems, including arterioles (A) with a muscular wall,thin-walled lymphatics (L), venules (V), and nerve bundles (NB)containing myelinated and unmyelinated nerves. Reproduced withpermission from Walton R, Leonard L, Sharawy M, Gangarosa L.Oral Surg 1979;48:545.

Figure 2-12 Pulpal fibroblasts showing spindle-shaped cyto-plasm. Plump nuclei (dark arrow) usually indicate active collagenformation. Condensed nucleus is in a “quiet” cell, often termed afibrocyte (open arrow). Pericytes (P) lie in close apposition to ves-sels and differentiate into other typical pulp cell types on demand.


Lymphocytes and Plasma Cells. These inflammato-ry cell types generally appear following invasion intothe area of injury by neutrophils. These cells are notnormally present in healthy pulp tissue but are associ-ated with injury and resultant immune responses—attempts to destroy, damage, or neutralize foreign sub-stance(s). Their presence would therefore indicate thepresence of a persistent irritant.

Mast Cells. Interestingly, mast cells are seldom inlarge numbers in normal, healthy pulps51 but are com-monly found in inflamed pulps.52,53 The granules ofthese cells contain histamine, a potent inflammatorymediator, and heparin. These cells release these gran-ules or degranulate into the surrounding tissue fluidduring inflammation.52

Since these cells are generally found near blood ves-sels, degranulation of mast cells releases histamineclose to vascular smooth muscle, causing vasodilation.This increases vessel permeability, allowing fluids andleukocytes to escape.

Odontoblasts. The principal cell of the dentin-forming layer, the odontoblast, is the first cell typeencountered as the pulp is approached from the dentin(Figure 2-13). These cells arise from peripheral mes-enchymal cells of the dental papilla during tooth devel-opment (see Structural Elements) and differentiate byacquiring the characteristic morphology of glycopro-tein synthesis and secretion54 (Figure 2-14).Glycoprotein forms the predentin matrix, which is ren-dered mineralizable by the odontoblast, a unique cellproducing a unique tissue, dentin. Synthesizing andsecretory activities render the odontoblast highly polar-ized, with synthesis occurring in the cell body and secre-tion from the odontoblastic process.

The cell body contains organelles that represent dif-ferent stages of secretion of collagen, glycoproteins, andcalcium salts.55 Matrix secretion precedes mineraliza-tion with these two events separated in time and spaceby the predentin. As happens in bone, the initial miner-al seeding of predentin at the dentinoenamel junction isby formation of “matrix vesicles.”56,57 Classic studies byWeinstock and colleagues,45,58,59 using an autoradi-ographic technique, have demonstrated the functionalsequence of matrix production and secretion. Thismaterial has recently been reviewed by Holland.60

In histologic sections viewed under a light micro-scope, odontoblasts appear to vary from tall, pseudos-tratified columnar cells in the coronal pulp (see Figure2-10) to a single row of cuboidal cells in radicular pulpto a flattened, almost squamous shape near theapex.61,62 These squamous cells often form an irregular,atubular dentin.

Scanning electron microscopy has provided a betterview of the external morphology of the odontoblasts(see Figure 2-10, C and D). The large nucleus is locatedin the base of the cell, giving it a pear-shaped appear-ance.63 From an exquisite scanning electron micro-scopic study, French dental scientists have demonstrat-ed that odontoblast cell bodies “appear tightly packedin the pulp horn and successively pear shaped, spindleshaped, club shaped, or globular from the crown to theapex”64 (Figure 2-15).

During dentin formation in the crown, the odonto-blasts are pushed inward to form the periphery of apulp chamber, the circumference of which is increas-ingly smaller than the original circumference at thedentinoenamel junction. This explains why the cells arepacked and palisaded into a pseudostratified appear-

Figure 2-13 Pseudostratified appearance of odontoblasts. Darkhorizontal line (arrow) delineates cell body from the odontoblasticprocesses and predentin and was once termed “pulpodentinalmembrane.” Ultrastructural examination has shown this to be aterminal cell web that forms a support and attachment areabetween adjoining cells. Reproduced with permission from WaltonR, Leonard L, Sharawy M, Gangarosa L. Oral Surg 1979;48:545.

ance of coronal odontoblasts. Conversely, because thespace is not so compressed in the radicular pulp, theodontoblasts maintain a columnar, cuboidal, or (in theapical region) squamous shape. Also, the resulting celland tubule density is much higher in the pulp chamberthan in the root pulp.65 This increased tubule density in

36 Endodontics

the chamber may explain the greater sensitivity andpermeability of the dentin of the crown.

The cell body manufactures the matrix material; thematerial is transported to and secreted from the odon-toblastic process. Classically, the odontoblastic processhas been described as extending from the cell body tothe dentinoenamel junction, a distance of 2 to 3 mm(ie, 2,000 to 3,000 µm). This concept was based on theobservations of many light microscopists using a vari-ety of special procedures and stains. 66 When dentinwas examined by electron microscopy, the odontoblas-tic process was determined to be limited to the innerthird of dentin, with the outer two-thirds of the tubuledevoid of processes or of nerves but filled with extra-cellular fluid.67–70 More recent investigations indicatethat odontoblastic processes may indeed extend to thedentinoenamel junction.71,72 However, tubular struc-tures in dentinal tubules are not necessarily odonto-blastic processes.73,74 Unequivocal identification can bedone only by identifying a trilaminar plasma mem-brane around the putative process using transmissionelectron microscopy.75,76 The extent of the odontoblas-tic process remains controversial.77

Therefore, modern interpretations of pulpal injuryfollowing conservative cavity preparation may not beattributable to amputation of odontoblastic processesbut to desiccation, heat, and osmotic effects. Further,dentin sensitivity may not be related to direct stimula-tion of either odontoblastic processes or nerves inperipheral dentin since the tubules may be devoid ofsuch structures in the periphery of dentin.

After initial dentin formation, the odontoblast, viaits process, can still modify dentin structure by produc-ing peritubular dentin. This is a hypermineralized cuffwith little organic matrix within the tubule, decreasingthe diameter of the tubule.78–80 When irritated, theodontoblast can accelerate peritubular dentin forma-

Figure 2-14 Odontoblasts, as viewed under the electron micro-scope, show organelles essential for protein synthesis, a plumpnucleus filled with euchromatin, and cytoplasm rich with roughendoplasmic reticulum (R) and a well-developed Golgi apparatus(G). (Courtesy of Dr. Dale Eisenmann.)

Figure 2-15 Diagram summarizing shape variation of odonto-blast cell bodies. A, Pulp horn (pear shaped); B, coronal midpulplevel (spindle shape); C, coronal midroot level (elongated clubshape); D, mid-third of root (short club shape); E, apical third ofroot (globules). Reproduced with permission from Marion D, et al.Oral Surg 1991;72:473.

A B C D E


tion to the point of complete occlusion of the tubule(Figure 2-16).81–83 When tubule occlusions extend overa large area, this is referred to as sclerotic dentin, com-monly found in teeth with cervical erosion.44

Alternatively, irritated odontoblasts can secrete col-lagen,84 amorphous material, or large crystals into thetubule lumen; these occlusions result in decreases indentin permeability to irritating substances.81–83

Although these secretions have been described as adefensive reaction by the odontoblast to protect itselfand the underlying pulp, this “protection” has neverbeen proved.

Extracellular. The dental pulp has most of its vol-ume primarily composed of fibers and ground substance.These form the body and integrity of the pulp organ.

Fibers. The morphology of collagen fibers, aprincipal constituent in the pulp, has been describedat the level of both light and electron microscopy. Atthe ultrastructural level, typical 640 angstrom band-ing or electron-dense periodicity provides positiveproof of collagen fiber identity.85 These fibers form aloose, reticular network to support other structuralelements of the pulp. Collagen is synthesized andsecreted by odontoblasts and fibroblasts. However, thetype of collagen secreted by odontoblasts to subse-quently mineralize differs from the collagen producedby pulpal fibroblasts, which normally does not calcify.They also differ not in basic structure but in thedegree of cross-linking, and in slight variation inhydroxylysine content.86

Tropocollagen is immature collagen fibers thatremain thin and stain black with silver nitrate,described in light microscopy as argyrophilic or reticu-lar fibrils. If tropocollagen molecules aggregate intolarger fibers, they no longer stain with silver and aregenerally termed “collagen fibers.” If several collagenfibers aggregate (cross-link) and grow more dense, theyare termed “collagen bundles.” Collagen generallybecomes more coarse (ie, develops more bundles) asthe patient ages. Age also seems to permit ectopic calci-fication of pulp connective tissue, ranging from thedevelopment of random calcifications to diffuse calcifi-cations87 to denticle (pulp stone) formation. Elastin,the only other fibrous connective tissue protein, isfound only in the walls of pulp arterioles.

Collagen has been described as having a uniquearrangement in the peripheral pulp; these bundles ofcollagen are termed von Korff ’s fibers. Most textbooksdescribe von Korff ’s fibers as being corkscrew-like andoriginating between odontoblasts to pass into thedentin matrix (Figure 2-17). The tight packing ofodontoblasts, predentin, capillaries, and nerves pro-duces very narrow spaces between and around odonto-blasts that can retain heavy metal stain (precipitates).Ten Cate’s electron microscopic studies of the distribu-tion of these precipitates demonstrated their presencein narrow intracellular tissue spaces.88 He claimed thatthey represented artifactual “stains” that were notattached to collagen fibers.88 However, more recentscanning electron microscopic studies (see Figure 2-10,

Figure 2-16 Mineralization of dentinal tubules in an aginghuman tooth. Electron micrograph of transparent root dentin froma 45-year-old person. The more densely mineralized peritubulardentin is white and the tubule itself is black. Two tubules are visiblein cross-section. The tubule on the left is almost completely occlud-ed. The progressive nature of mineralization is evident in the tubuleon the right. (Courtesy of Dr. John Nalbandian.)

Figure 2-17 Peripheral pulp. The corkscrew-like structures (vonKorff ’s fibers) reportedly are collagen fibers that originate in thepulp, pass between odontoblasts, and are incorporated into pre-dentin. That these are collagen fibers is disputed. Reproduced withpermission from Bernick S.155

D) of the predentin-pulpal border demonstratingscrew-like fibrous material have stimulated new specu-lation that von Korff ’s fibers are real structures.63

Ground Substance. This structureless mass,gel-like in consistency, makes up the bulk of the pulporgan. It occupies the space between formed elements.The ground substance resembles that of other areolar,fibrous connective tissues, consisting primarily of com-plexes of proteins and carbohydrates and water. Morespecifically, these complexes are composed of combina-tions of glycosaminoglycans, that is, hyaluronic acid,chondroitin sulfate, and other glycoproteins.89,90 Theground substance surrounds and supports structuresand is the medium through which metabolites andwaste products are transported to and from cells andvessels. Aging of the pulp alters the ground substance,91

although there is no substantive proof that these alter-ations significantly inhibit pulp functions.

Supportive Elements.Pulpal Blood Supply. Numerous investigators have

described the blood supply of the dental pulp.92–95

Because the pulp itself is small, pulp blood vessels donot reach a large size. At the apex and extendingthrough the central pulp, one or more arterioles branchinto smaller terminal arterioles or metarterioles that aredirected peripherally (Figure 2-18, A). Before the arte-rioles break up into capillary beds, arteriovenous anas-tomoses often arise to connect the arteriole directly toa venule.96 These arteriole-venule shunts are identifiedby the presence of irregularly oriented myoepitheli-um-like cells surrounding them and by the cuboidalnature of the cells lining their lumen.97 The classicdescription of microcirculatory beds includes capillar-ies that branch off arterioles at right angles (Figure 2-18, B). Unfortunately, no such structures have beenfound in human pulps. Instead, arterioles branch intoterminal arterioles, which, in turn, give rise to capillar-ies (Figure 2-19).

Capillary density is highest in the subodontoblasticregion with loops passing between odontoblasts(Figure 2-20).98–100 In the subodontoblastic region,capillaries with fenestrations occur frequently and reg-ularly in both primary and permanent teeth (Figure 2-21). The fenestrae (“windows”) are spanned by a thindiaphragm of plasma membrane. The frequency offenestration falls off rapidly when examining centralcapillaries, being as low as 4% in the coronal pulp.98,101

Capillaries empty into small venules that connectwith fewer and successively larger venules. At the apex,multiple venules exit the pulp. These venules connectwith vessels that drain the periodontal ligament oradjacent alveolar bone. The vessels of the pulp have

38 Endodontics

Figure 2-18 A, Perfused pulp of dog premolar showing the sizeand location of vessels. Larger central vessels are arterioles andvenules. Peripherally directed are smaller metarterioles that branchinto the rich network of looping capillaries of peripheral pulp. B,Schematic diagram of classic microcirculatory vascular bed thatwould represent a region of central and peripheral vessels as seen inA. Arterioles are invested by a continuous layer of smooth musclecells. Metarterioles have discontinuous clusters of smooth musclewith capillaries branching directly off metarterioles. Precapillarysmooth muscle sphincters are strategically located to control capil-lary blood flow. True capillaries lack smooth muscle. Arteriovenousshunts represent direct connections between arterioles and venules.Their muscles are innervated by sympathetic nerve fibers. A repro-duced with permission from Seltzer S, Bender IB. The dental pulp.2nd ed. Philadelphia: JB Lippincott; 1975. p. 106.

A

B


thinner muscular walls (tunica media) than vessels ofcomparable diameter in other parts of the body.Undoubtedly, this is an adaptation to the surroundingprotective and unyielding walls.102 Kim and his associ-ates have obtained evidence that suggests that mostvasodilating agents induce only a transient, briefincrease in pulpal blood flow followed by a decrease inblood flow owing to collapse of local venules.103

Apparently, the vasodilation either directly impinges

on venules or permits transudation of fluid across cap-illaries that indirectly compresses the thin-walledvenules in the low-compliance system of the pulpchamber.

The above-described general vascular architecture isfound in each tooth root. Alternate blood supply isavailable to multicanaled teeth, with the resulting richanastomoses in the chamber. The occasional vesselsthat communicate via accessory canals have not been

Figure 2-19 Corrosion resin casts of the pulp vessels of a dog pre-molar. A, Higher magnification of the region enclosed by the squarelabeled A in C demonstrates many hairpin capillary loops withinthe pulp horn (×300 original magnification). B, Higher magnifica-tion of the area enclosed by the square labeled B in C. Arterioles (a)arborize from artery to form a capillary (c) network on the surfaceof the radicular pulp. Venule (V) is about 50 micrometers in diam-eter. Arterioles are about 10 micrometers in diameter. Superficialcapillary network demonstrates cross-fence shape. C, Montage ofthe entire pulp made from multiple, overlapping scanning electronmicrographs (×50 original magnification). The three projections inthe coronal region represent three pulp horns, apical foramen (af).(Courtesy of Drs. K. Takahashi, Y. Kishi, and S. Kim.)

CA

B

demonstrated to contribute significantly as a source ofcollateral circulation.

Lymphatics. The presence of pulpal lymphatics isdisputed.104,105 However, lymphatics have been identi-fied in the pulp at the ultrastructural98 and histologiclevels by the absence of red blood cells in their lumina,the lack of overlapping of endothelial margins, and theabsence of a basal lamina.87,98,106–108 They arise as lym-phatic capillaries in the peripheral pulp zone (Figure 2-22) and join other lymph capillaries to form collectingvessels.87 These vessels unite with progressively largerlymphatic channels that pass through the apex with theother vasculature. Numerous authors, using both histo-logic and functional methods, have described extensiveanastomoses between lymph vessels of the pulp, peri-odontal ligament, and alveolar bone.108–114

Functional Implications. The presence of arteriove-nous shunts32,96 in the pulp provides the opportunityfor blood to shunt115,116 past capillary beds since thesearteriole-venule connections are “upstream” from thecapillaries. Alternatively, the arteriole-venule shuntscould remain nearly closed (in a constricted state), andmost of the blood would pass peripherally in the pulpto perfuse capillaries and the cells that they support.115

It has been suggested that the distribution of bloodflow might change during pulp inflammation.117

Increased dilation of arteriole-venule shunts may pro-duce “hyperemia,” in which more blood vessels thannormal are open and filled with blood cells; this mayindicate more rapid blood flow or represent partial sta-sis. Further, this dilation of arteriole-venule shunts may“steal” blood from capillary beds, causing accumula-tion of waste products.

40 Endodontics

Capillary fenestration may indicate that these capil-laries are more permeable to large molecules or thatthey allow more rapid fluid movement across theendothelium.118 However, studies on pulp capillaries

Figure 2-20 Electron micrograph of subodontoblastic capillarylooping between odontoblasts. Portions of several red blood cells areseen within the lumen. Reproduced with permission from Avery J.100

Figure 2-21 A, Electron micrograph of cross-section of the capil-lary loop passing between and closely surrounded by odontoblasts.Inset shows higher magnification of a portion of endothelial wall ofthe capillary demonstrating fenestrations (arrow). B, Subodonto-blastic capillary with large nucleus of endothelial cell impinging onlumen. Plasticity of red blood cell (black) allows it to adapt to irreg-ular contours of lumen. Prominent basement membrane encirclesthe periphery of the cell. (A courtesy of Dr. K. Josephsen, Denmark;B courtesy of Dr. Robert Rapp.)

A

B


suggest a lower than normal permeability to large mol-ecules. On the other hand, a higher rate of fluid move-ment has not been ruled out. Increased transudation ofplasma and polymorphonuclear neutrophil leukocytesfrom the circulation occurs most often in venules50

rather than capillaries.The structural identification of lymph capillar-

ies87,98,107 complements the functional studies ofWalton and Langeland,108 who demonstrated that sub-stances placed in the pulp chamber can be found inregional lymph nodes. The open endothelial marginsand incomplete basal lamina permit entry of large mol-ecules and even bacteria. The fact that materials placedon pulps can migrate to lymph nodes119 indicates thepossibility of immunologic reactions to substances thatenter the pulp.120 Bernick described the appearance oflymphatics in the inflamed pulp and surmised thattheir function is to remove the excess fluid and debristhat accompanies inflammation.87

Unfortunately for the pulp, the lymphatics may col-lapse as pulp pressure rises, thus inhibiting removal of

irritants and fluid. Clearly, more investigation isrequired before one can understand how lymphaticfunction is disturbed in pulp inflammatory conditions.The anastomoses of pulpal, periodontal, and alveolarlymphatics may be important routes for the spread ofpulpal inflammation into adjacent tissues during theremoval of irritants and fluid from the pulp. Thesestructural interrelationships have not received theattention they deserve. Finally, the extent and degree ofanastomoses of apical venules with those of the peri-odontal ligament and alveolar bone need investiga-tion.92 Vessels may provide a route for local anestheticmovement during intraosseous or periodontal liga-ment injections121 rather than the fluid “dissecting”through perivascular tissue spaces.122 These same path-ways have been implicated as routes of spread ofinflammation from pulp to periodontal ligamentand/or bone and vice versa.

Nerves. Several nerve bundles, each containingnumerous unmyelinated and myelinated nerves, passinto each root via the apical foramen. The majority areunmyelinated nerves,123–125 most of which are part ofthe sympathetic division of the autonomic nervous sys-tem; these have been shown to cause reductions in pulpblood flow when stimulated.126,127 The remainingnerves are myelinated sensory nerves of the trigeminalsystem (Figure 2-23).

The myelinated nerve fibers branch extensivelybeneath the cell-rich zone to form the so-called plexusof Raschkow (Figure 2-24). From here, many fibers losetheir myelin sheath and pass through the cell-free zoneto terminate as receptors or as free nerve endings nearodontoblasts (Figure 2-25); others pass between odon-toblasts to travel a short distance up the dentinal tubulesadjacent to odontoblastic processes.128 The nerve end-ings terminate far short of the dentinoenamel junction;rather, endings are found only in tubules of the innerdentin and predentin, on or between odontoblasts.129

Byers has found that intradental nerves pass approxi-mately 100 µm into the tubules, regardless of the dentinthickness, in a wide variety of animal species.130 Perhapsnerve fibers cannot be nourished beyond a 100 µm dif-fusion distance. Some sensory axons exhibit terminalaborizations that innervate up to 100 dentinaltubules.130 Significantly, sensory nerves of the pulprespond to noxious stimuli with pain sensation only,regardless of the stimulus. This pain is producedwhether the stimulus is applied to dentin or the pulp.

Cavity preparation in the unanesthetized tooth ispainful at any depth of dentin. How can this occur ifthere are no sensory nerves in the outer two-thirds ofdentin? The answer probably lies in the hydrodynamic

Figure 2-22 Lymphatic capillary arising and collecting from with-in the odontoblast-subodontoblast region of a human pulp. Arrowsdelineate margins of the vessel, draining toward the central pulp.Reproduced with permission from Bernick S.87

42 Endodontics

Figure 2-23 Schematic drawing showing sensory nerve location in pulp and dentin. Percentage of innervated tubules at regions A through Dis indicated (left). Px = plexus of Raschkow; cfz = cell-free zone; O = odontoblasts; p = predentin. Reproduced with permission from Byers M.144

Figure 2-24 Branching of nerve bundles as they approach thesubodontoblastic region (plexus of Raschkow). (Courtesy of Dr.James Avery.)

Figure 2-25 Nerve terminal (arrow) located between adjacentodontoblasts near calcifying dentin. Large number of vesicles ischaracteristic of nerve terminal. Terminal is closely applied to theadjacent odontoblastic process; this does not, however, represent asynapse. (Courtesy of Dr. James Avery.)


theory in which fluid movement within tubules stimu-lates distant sensory nerve endings (see Byers et al andAvery128–131 for reviews).

Highly organized junctions have been demonstratedbetween some nerve fibers and odontoblasts.132–136

Although they do not appear to be typical synapticjunctions, their existence must be functional. It isunclear whether the activity is sensory or motor.

An additional function of sympathetic nerves is thepossible regulation of the rate of tooth eruption.Sympathetic nerve activity influences local blood flowand tissue pressure by opening or closing arteriovenousshunts as well as arteriolar blood flow; this may sec-ondarily affect eruptive pressure.137 Activation of sym-pathetic fibers not only reduces pulpal blood flow138

but also decreases the excitability of intradentalnerves.139 Thus, there is a very intimate relationshipbetween pulpal nerves and their excitability and localblood flow.140

Numbers and concentrations of nerves vary withthe stage of tooth development and also with location.Fearnhead and others have reported that very fewnerves appear in the human pulp prior to tooth erup-tion.41,141,142 After eruption, the highest number ofnerves is found in the pulp horns (about 40% of thetubules are “innervated”). The number of nerves pertubule drops off to about 4.8% in the more lateralparts of the coronal dentin to less than 1% in the cer-vical region (see Figure 2-23), with only an occasionalnerve in radicular dentin.143 Patterns of branchingnerves seen with the light microscope would confirmnumbers of nerves at different levels. There is littlebranching off the main nerve bundles until the coro-nal pulp. Regions of sensitivity also correlate in thatcoronal pulp and dentin are more painful to stimulithan are radicular pulp and dentin. The same stimuliapplied to dentin were described as “sharp” whenapplied to coronal dentin but “dull” when applied toradicular dentin.144 Restorative procedures in rat teethcause sprouting of pulpal and intradental nerves thatmay modify both dentin sensitivity145 and localinflammatory reactions.146

Interestingly, removal of the pulp by extraction of thetooth or by pulpectomy and, presumably, pulpotomyresults in the successive degeneration of the cell bodieslocated in the spinal nucleus of the trigeminal nerve, themain sensory ganglion, and the peripheral nerve lead-ing to the tooth in the socket.147 Bernick observed theeffects of caries and restorations on underlying nervesin the pulp.148 He found a degeneration of the sub-odontoblastic plexus of nerves associated with the pro-duction of irritation dentin. He concluded that “the ter-

minal nerves in the injured pulp are sensitive to thenoxious products of caries and the restorative proce-dures. An apparent decrease in sensitivity results inrestored teeth.” The lack of sensitivity that accompaniesthe caries process may be attributable, at least partially,to degeneration of underlying nerves.

Calcifications. Basically, there are two distincttypes of pulpal calcifications: formed structures com-monly known as pulp stones (denticles) and tiny crys-talline masses generally termed diffuse (linear) calcifi-cations (Figure 2-26). Pulp stones seem to be foundpredominantly in the coronal pulp, whereas the calcifi-cations found in radicular pulp seem to be of the dif-fuse variety.149

Calcifications are common in the dental pulp, with atendency to increase with age and irritation. It has beenspeculated that these calcifications may aggravate oreven incite inflammation of pulp or may elicit pain bypressing on structures; however, these speculationshave not been proved and are improbable. Althoughthese calcifications are not pathologic, their presenceunder certain conditions may be an aid in diagnosis ofpulpal disease. Moreover, their bulk and position mayinterfere with endodontic treatment.

Pulp Stones. These discrete calcific masses appearwith frequency in mature teeth.150 Although there isincreased incidence with age, they are not uncommon

Figure 2-26 Uninflamed pulp. Typical pattern of calcifications.Larger pulp stones in the chamber blend into linear diffuse calcifica-tions in the canal. Reproduced with permission from Bernick S.155

in young teeth. It has also been demonstrated that theiroccurrence and size often increase with external irrita-tion.151 Pulp stones also may arise spontaneously; theirpresence has been identified on radiographs (Figure 2-27) and, on histologic examination, even in impactedteeth.152 Interestingly, there appears to be a predisposi-tion for pulp stone formation in certain individuals,possibly a familial trait.

Pulp stones have been classified as two types, true orfalse. However, recent careful histologic examinationhas discounted the true pulp stone. Supposedly, truepulp stones are islands of dentin, demonstratingtubules and formative odontoblasts on their surface.However, serial sectioning has shown that these are notislands but peninsulas—extrusions from dentinwalls.152,153 Therefore, the term “denticle,” whichwould imply dentin structure, is a misnomer. The term“pulp stone” is more correct, particularly because the“false” pulp stone so closely resembles gallstones andkidney or ureter stones.

Pulp stones, like other types of stones, are formedfrom clearly concentric or diffuse layers of calcified tis-sue on a matrix that seems to consist primarily of col-lagen.154 Their structure may help explain their origin;it has been shown that potential nidi of pulp stonesmay occur in the sheaths associated with blood vessels(Figure 2-28) and nerves.155 Other potential nidi arecalcifications of thrombi in vessels or calcification ofclumps of necrotic cells.153 Whatever the nidus, growthis by incremental layering of a matrix that quicklyacquires mineral salts.

44 Endodontics

Pulp stones are also classified according to location.“Free” stones are those that are islands, “attached”stones are free pulp stones that have become fused withthe continuously growing dentin, and “embedded”stones are formerly attached stones that have nowbecome surrounded by dentin.

Pulp stones may be important to the clinician whoattempts access preparation or to negotiate canals.Either free or attached denticles may attain large sizeand occupy considerable volume of the coronal pulp(Figure 2-29). Their presence may alter the internalanatomy and confuse the operator by obscuring, butnot totally blocking, the orifice of the canal. Attacheddenticles may deflect or engage the tip of exploringinstruments in the canals, thus preventing their easypassage down the canal.156

Pulp stones of sufficient size are readily visible onradiographs, although the majority are too small to beseen except on histologic examination. The large, dis-crete masses, occasionally appearing to nearly fill thechamber (Figure 2-30), are likely to be those of naturaloccurrence. The chamber that appears to have a diffuseand obscure outline may represent a pulp that has beensubjected to a persistent irritant and has responded byforming large numbers of irregular pulp stones. Thisfinding is a diagnostic aid and indicates a pulp exposedto a persistent chronic irritant.

Diffuse Calcifications. Also known as linear calci-fications because of their longitudinal orientation,

Figure 2-27 Second molar demonstrates chamber nearly filledwith pulp stones (arrow). Stones may have arisen spontaneously,or their presence may indicate chronic irritation and inflamma-tion from caries and/or deep restoration. (Courtesy of Dr. G.Norman Smith.)

Figure 2-28 Calcification of the sheath surrounding this smallvessel may form a nidus for growth of a larger calcified structure, apulp stone. Reproduced with permission from Bernick S. J Dent Res1967;46:544.


these are common pulp findings. They may appear inany area of the pulp but predominate in the radicularregion.157 Their form is that of tiny calcifiedspicules,156 usually aligned close to blood vessels andnerves or to collagen bundles (see Figure 2-26).Because of their size and dispersion, they are not visi-ble in radiographs and are seen only on histologic spec-imens. Like pulp stones, diffuse calcifications also tendto increase with age and with irritation but otherwisehave no known clinical significance.

PULP CHANGES WITH AGE

Teeth age, not only with the passage of time but alsounder the stimulus of function and irritation.Therefore, age is a chronologic occurrence, but evenmore importantly, an “aged” tooth may represent a pre-mature response to the abuses of caries, extensiverestorative procedures, and inflicted trauma. Since thepulp reacts to its environment and is in intimate con-tact with dentin, it responds to abuses by altering theanatomy of its internal structures and surroundinghard tissue.

Dimensional

With time and/or injury, the pulp volume decreases byforming additional calcified tissues on the walls (seeFigure 2-30). Ordinarily, with time, formation ofdentin continues, with the greatest increase on thefloor of the chamber of posterior teeth158 (Figure 2-31) and on the incisal of anterior teeth. In such teeth,the location of the pulp chamber and/or root canalsmay be difficult. In anterior teeth, the clinician mayhave to search cervically to locate a remnant of thechamber. In molars, dentin formation may have ren-dered the chamber almost disk-like; while searching, itis easy to inadvertently pass a bur through the flat-tened chamber (Figure 2-32). If the preparation iscontinued, the next hemorrhage encountered will arise

Figure 2-29 Large pulp stone may have been formed by growthand fusion of smaller stones such as those below it. Examination ofother serial sections may show that this apparently “free” pulp stoneis actually attached to dentin walls. Reproduced with permissionfrom Bernick S.155

Figure 2-30 Large pulp stones may fill and nearly obscure the entirechamber. In some areas, the margins of the stone have fused with thedentin walls. Reproduced with permission from Bernick S.155

Figure 2-31 Pattern of dentin formation in “aged” posterior toothfrom a 60-year-old patient. Typically irregular hard tissue apposi-tion is greatest on the floor, decreasing chamber depth. (Courtesy ofDr. Sol Bernick.)

from the furcation, not from the chamber. Carefulexamination of radiographs to identify chamber sizeand location, followed by measurements of the occlu-sochamber distance, will prevent this mishap.Irritation dentin formation will also alter internalanatomy. Therefore, when the dentin has been violat-ed by caries or by attrition, one should expectincreased amounts of hard tissue in the underlyingpulp. Irritation dentin may occasionally be extensiveenough to obscure or fill large areas of the chamber.

Structural

Although exacting quantitative studies have not beenpublished, there is agreement that the number of cellsdecreases and the fibrous component increases withaging of the pulp (Figure 2-33).159 The increased fibro-sis with time is not from continued formation of colla-gen but rather may be attributable to a persistence ofconnective tissue sheaths in an increasingly narrowedpulp space.155,160

Bernick observed a decrease in the number of bloodvessels155 and nerves161 supplying the aging pulp, not-ing that many of the arteries demonstrated arterioscle-rotic changes similar to those seen in other tissues161

(Figure 2-34). These changes involve decreases inlumen size with intimal thickening and hyperplasia ofelastic fibers in the media. Also common is calcificationof arterioles and precapillaries.161 Although thesestructural changes are described, it is not clear whetherthe vascular and neural changes alter the function ofthe older pulp.

46 Endodontics

Not only do cells decrease in number, notablyfibroblasts and odontoblasts, but the remaining cellsare likely to appear relatively inactive. These ordinarilyactive cells demonstrate fewer organelles associatedwith synthesis and secretion.1

Figure 2-32 Disk-like chamber (arrow) is a result of hard tissueapposition on the floor and roof. The center of the chamber is difficultto locate. An access preparation should be started by locating the largeorifice of the distal canal first. (Courtesy of Dr. G. Norman Smith.)

Figure 2-33 Age changes in cross-sections of human pulp. A,Young pulp with characteristic cellularity and relatively small scat-tered fibrous components of central pulp. B, Acellularity and largefiber bundles are common findings in mature pulps. (Courtesy ofDr. Dennis Weber.)

Figure 2-34 Cross-section of small arterioles in the apical third ofpulp from an older person. The lumina are decreased in size, show-ing thickening of the tunica intima and hyperplasia of the tunicamedia—changes characteristic of arteriosclerosis. Reproduced withpermission from Bernick S. J Dent Res 1967;46:544.

A

B


“Regressive” Changes

The term “regressive” is defined as a condition ofdecreased functional capability or of returning to a moreprimitive state. Older pulps have been described asregressive and as having a decreased ability to combatand recover from injury. This has been surmised becauseolder pulps have fewer cells, a less extensive vasculature,and increased fibrous elements. In fact, there have neverbeen experiments proving that aged pulps are more sus-ceptible to irritants or less able to recover. Until thesehave been conclusively demonstrated, the term “regres-sion” is not appropriate, and the dentist should notassume that pulps in older individuals are less likely torespond favorably than are younger pulps.

PULPAL RESPONSE TO INFLAMMATION

Pulp structures and functions are altered, often radical-ly, by injury and resulting inflammation. As a part of theinflammatory response, neutrophilic leukocytes arechemotactically attracted to the site. Bacteria or dyingpulp cells are phagocytosed, causing release of potentlysosomal enzymes. These enzymes may attack sur-rounding normal tissue, resulting in additional damage.

For instance, by-products of the hydrolysis of colla-gen and fibrin may act as kinins, producing vasodila-tion and increased vascular permeability.162,163

Escaping fluid tends to accumulate in the pulp intersti-tial space, but because the space is confined, the pres-sure within the pulp chamber rises. This elevated tissuepressure produces profound, deleterious effects on thelocal microcirculation. When local tissue pressureexceeds local venous pressure, the local veins tend tocollapse, increasing their resistance; hence blood willflow away from this area of high tissue pressure as itseeks areas of lower resistance. This process of blooddiversion can be illustrated by applying slight pressureto the end of a fingernail. As the pressure increases, thenail bed blanches as blood is squeezed out of the localvessels, and new blood is prevented from flowingthrough this area of elevated tissue pressure. Persistentpressure continues to compromise circulation. Theconsequences of reduced local blood flow are minor innormal tissue but disastrous in inflamed tissue becausethe compromised circulation allows the accumulationof irritants such as injurious enzymes, chemotoxic fac-tors, and bacterial toxins.

This event may lead to the development of the “com-partment syndrome,”164–166 a condition in which ele-vated tissue pressure in a confined space alters struc-ture and severely depresses function of tissues withinthat space. Depressed function often leads to cell death,which, in turn, produces inflammation resulting in

fluid escape and increased pressure within the com-partment. The increased tissue pressure collapses veins,thereby increasing the resistance to blood flow throughcapillaries. Blood is then shunted from areas of hightissue pressure to more “normal” areas. Thus, a viciouscycle is produced in which inflamed regions tend tobecome more inflamed because they tend to limit theirown local nutrient blood flow (Figure 2-35).

This is not to say that the pulp “strangulation” theo-ry is valid. As shown by Van Hassel,167 and more recent-ly by Nahri168 and Tönder and Kvinnsland,169 pressuresare not readily transmitted throughout the pulp.Therefore, inflammation and increased pressure in thecoronal pulp will not collapse veins in the apical region.Pulps physiologically have multiple compartmentsthroughout. It is as if small volumes of pulp tissue areenclosed in separate connective tissue sheaths, each ofwhich can contain local elevations in tissue pressure.Although no histologic evidence exists to support thisnotion, these functional compartments may breakdown individually to become necrotic and may coalesceto form microabscesses.

The recent micropuncture work by Tönder andKvinnsland demonstrated that there are highly local-ized elevations in interstitial tissue pressure in inflamedpulp.169 This is thought by some to be caused by therelease of vasoactive neuropeptides such as substance Pand calcitonin gene–related peptide, both found inpulp nerve fibers.170 During pulpal inflammation,there is an increase in the number of calcitoningene–related peptide–containing nerves in areas previ-ously devoid of nerves. The release of these peptidesseems to promote and sustain inflammation, prompt-ing some to call it neurogenic inflammation.171

PULPODENTINAL PHYSIOLOGY

As long as dentin is covered peripherally by enamel oncoronal surfaces and cementum on radicular surfaces,the dental pulp will generally remain healthy for life,unless the apical blood supply is disrupted by excessiveorthodontic forces or severe impact trauma. Mostpathologic pulp conditions begin with the removal ofone or both of these protective barriers via caries, frac-tures, or abrasion. The result is the communication ofpulp soft tissue with the oral cavity via dentinaltubules, as has been demonstrated by dye penetrationstudies172 and radioactive tracer experiments.173

It is apparent that substances easily permeate dentin,permitting thermal, osmotic, and chemical insults toact on the pulpal constituents. The initial stages involvestimulation or irritation of odontoblasts and may pro-ceed to inflammation and often to tissue destruction.

To understand how these steps may lead to pulpdamage, the pulpodentinal complex will be examinedin its separate forms.

Dentin Structure

Dentin is a calcified connective tissue penetrated bymillions of tubules; their density varies from 40,000 to70,000 tubules per square mm.174,175 Tubules are from1 µm in diameter at the dentinoenamel junction to 3µm at their pulpal surface and contain fluid that has acomposition similar to extracellular fluid.176 If thefluid becomes contaminated, for example, with cariousbacterial endotoxins and exotoxins, then it develops areservoir of injurious agents that can permeate throughdentin to the pulp to initiate inflammation.177 It is use-ful to understand the important variables that controldentin permeability.

Dentin Permeability. Dentinal tubules in thecoronal dentin converge from the dentinoenamel junc-tion to the pulp chamber.178 This tends to concentrateor focus permeating substances into a smaller area attheir terminus in the pulp. The surface area occupiedby tubules at different levels indicates the effect oftubule density and diameter. One can calculate fromGarberoglio and Brännström’s175 observations that the

48 Endodontics

area of dentin occupied by tubules is only 1% at thedentinoenamel junction and increases to 45% at thepulp chamber. The clinical implications of this areenormous. As dentin becomes exposed to increasingdepths by restorative procedures, attrition, or disease,the remaining dentin becomes increasinglypermeable.179,180 Thus, dentin removal, although nec-essary, renders the pulp more susceptible to chemicalor bacterial irritation. This functional consequence oftubule area is also responsible for the decrease in dentinmicrohardness closer to the pulp181,182; as tubule den-sity increases, the amount of calcified matrix betweenthe tubules decreases. This relative softness of thedentin lining the pulp chamber somewhat facilitatescanal enlargement during endodontic treatment.183

Overall dentin permeability is directly proportionalto the total surface area of exposed dentin. Obviously, aleaking restoration over a full crown preparation pro-vides more diffusional surface for bacterial productsthan would a small occlusal restoration.184 Restorationsrequiring extensive and deep removal of dentin (ie,preparation for a full crown) would open more andlarger tubules and increase the rate of injurious sub-stances diffusing from the surface to the pulp—thus theimportance of “remaining dentin thickness.”185,186 The

Figure 2-35 Vicious cycle of pulpalinflammation, which begins with irri-tation (top), leads to a localizedresponse, and may progress to a lesionof increasing severity and eventualirreversible pulpitis.


permeability of the root is 10 to 20 times less than thatof a similar thickness of coronal dentin.187 This mayaccount for the lack of pulpal reactions to periodontaltherapy that removes cementum and exposes rootdentin to the oral cavity.

Recent evidence indicates that dentin permeability isnot constant after cavity preparation. In dogs, dentinpermeability fell over 75% in the first 6 hours followingcavity preparation.188 Although there were no histolog-ic correlates of the decreased permeability, dogs deplet-ed of their plasma fibrinogen did not decrease theirdentin permeability following cavity preparation.189

The authors speculated that the irritation to pulpalblood vessels caused by cavity preparation increased theleakage of plasma proteins from pulpal vessels out intothe dentinal tubules, where they absorb to the dentin,decreasing permeability. Future study of this phenome-non is required to determine if it occurs in humans.

The character of the dentin surface can also modifydentin permeability. Two extremes are possible: tubulesthat are completely open, as seen in freshly fractured190 oracid-etched dentin,191 and tubules that are closed eitheranatomically66 or with microcrystalline debris.192 Thisdebris creates the “smear layer” (Figure 2-36), whichforms on dentin surfaces whenever they are cut with

either hand or rotary instruments.193 The smear layerprevents bacterial penetration194,195 but permits a widerange of molecules to readily permeate dentin. Smallmolecules permeate much faster than large molecules.Smear layers are often slowly dissolved over months toyears as oral fluids percolate around microleakage chan-nels between restorative materials and the tooth.196

Removal of the “smear layer” by acid etching or chelationincreases dentin permeability197 because the microcrys-talline debris no longer restricts diffusion of irritants andalso permits bacteria to penetrate into dentin.198 There isconsiderable debate as to whether smear layers created inthe root canal during biomechanical preparation (Figure2-37) should be removed.199 Its removal may increase thequality of the seal between endodontic filling materialsand root dentin. It may also increase the bond strength ofresin posts.200

Pulp Metabolism. The rate at which pulpal cellsare metabolizing can be quantitated by measuring theirrate of oxygen consumption, CO2 liberation, or lacticacid production.201 Fisher and colleagues reported thatzinc oxide–eugenol (ZOE) cement, eugenol, calciumhydroxide, silver amalgam, and procaine all depressedpulp oxygen consumption.202 Shalla and Fisherdemonstrated that lowering the medium pH of pulp

Figure 2-36 Schematic representation of theinterface of dentin and restorative material. Theglobular constituents of the smear layer havebeen exaggerated out of proportion for empha-sis. Reproduced with permission from PashleyDH.193 Oper Dent 1984;3:13.

cells below 6.8 caused a progressive decrease in oxygenconsumption.203 This undoubtedly occurs during thedevelopment of pulp abscesses. Even though pulp res-piration may decrease in an acid environment, Fisherand Walters have shown that bovine pulp has a veryactive ability to produce energy through anaerobic gly-colysis.204 Oxygen consumption has also been meas-ured in dental pulp tissue using an oxygen electrode.205

A more sensitive technique has recently been appliedto studying pulp respiration.206–208 Pulp tissue wasplaced in 14C-labeled substrates such as succinate andmeasured the rate of appearance of 14CO2 from thereaction vessel. Using this technique, reduced pulpmetabolism was demonstrated when ZOE cement,Dycal, Cavitec, and Sargenti’s formula/N2 wereused.206 It was also reported that the application oforthodontic force to human premolars for 3 days led toa 27% reduction in pulp respiration.207 The depressanteffects of eugenol on pulp respiration were reported aswell.208 Similar results were recently reported byHume.209,210 Pulpal irritation generally causes elevatedtissue levels of cyclooxygenase products. Eugenol inZOE cement has been shown to block this reaction.211

Pulp Reaction to Permeating Substances. Whathappens when permeating substances reach the pulpchamber? Although bacteria may not actually passthrough dentin, their by-products212,213 have beenshown to cause severe pulp reaction.177,212,214 Thebroad spectrum of pulp reaction, from no inflamma-

50 Endodontics

tion to abscess formation, may be related to the con-centration of these injurious substances in the pulp.Although exposed dentin may permit substances topermeate, their concentrations may not reach levelshigh enough to trigger the cascade of events associatedwith inflammation. This would indicate that the inter-stitial fluid concentration of these substances can bemaintained at vanishingly low concentrations. As longas the rate of pulp blood flow is normal, the microcir-culation is very efficient at removing substances diffus-ing across dentin to the pulp chamber.184 There isenough blood flowing through the pulp each minute tocompletely replace between 40 and 100% of the bloodvolume of the pulp.215 Since blood is confined to thevasculature, which comprises only about 7% of thetotal pulpal volume,215,216 the blood volume of thepulp is replaced 5 to 14 times each minute.

If pulpal blood flow is reduced,217–230 there will be aresultant rise in the interstitial fluid concentration ofsubstances that permeated across dentin.184 Theincreased concentration of injurious agents maydegranulate mast cells,49,50 release histamine231 or sub-stance P,232–236 produce bradykinin,237 or activate plas-ma proteins.238,239 All of these effects would initiateinflammation. The endogenous mediators of inflam-mation produce arteriolar vasodilation, elevated capil-lary hydrostatic pressure, increased leakage of plasmaproteins into the pulp interstitium,240 and increasedpulp tissue pressure.167,169,241 These events, by causingcollapse of local venules, lead to a further reduction inpulp blood flow,242 with an even higher interstitial con-centration of irritants; thus, a vicious cycle243 is createdthat may terminate in pulp death (see Figure 2-35).

Techniques for accurately measuring pulp tissuepressures were developed in the 1960s.244–248 Thesemethods all involve drilling carefully through theenamel and dentin to tap into the pulp chamber.Recently, several indirect methods of measuring pulppressure through intact dentin have been devised. Onegroup measured the pressure in a chamber cementedon cat dentin necessary to prevent outward movementof fluid as 15 cm H2O.249 Ciucchi et al, using the sametechnique in humans, reported a normal pulp pressureof 14 cm H2O (10.4 mm Hg), far below systemic bloodpressure but close to pulp capillary pressure (Figure 2-38).250 Recent direct measurements of pulpal intersti-tial fluid pressures by micropuncture have given pres-sures of 6 to 10 mm Hg. However, they were done onpulps exposed to the atmosphere.169

Pulp blood flow has been measured by numerousauthors using many different techniques.251–254

Recently, Gazelius and his associates reported the use of

Figure 2-37 Scanning electron micrograph of root canal dentintreated with 5% NaOCl and 17% EDTA (ethylenediamine-tetraacetic acid) to remove pulpal tissue and smear layer. A number8 file drawn over the clean surface in the middle of the field createsa smear layer (×2,000 original magnification). Reproduced withpermission from Goldman M et al.199


a laser Doppler blood flowmeter that was sensitiveenough to measure changes in pulpal blood flow inintact human teeth.253 This method has begun to beused in pulp biology research.138 Blood flow in the pulpfalls in direct proportion to any increase in pulp tissuepressure. Van Hassel,167 Stenvik and colleagues,241 andTönder and Kvinnsland169 reported that pulp tissuepressure is elevated in pulpitis but that the elevation islocalized within specific regions of the pulp, being nor-mal in noninflamed areas. The localized reduction inpulp blood flow, however, allows the accumulation ofmediators of inflammation, which, in turn, causes aspread in the elevation of tissue pressure, reducing pulpblood flow to a larger volume of pulp, etc.167,243 Theelevated pulp tissue pressure causes dull, aching, poor-ly localized pulp pain, a type of pain that differs fromthe brief, sharp, well-localized dentinal pain that is pos-tulated to be caused by fluid movement within dentin.3

Accordingly, when teeth with elevated pulp pressuresare opened to the pulp, the pain generally subsides rap-idly as tissue pressures rapidly fall.

Dentin Sensitivity. Clinicians recognize that dentinis exquisitely sensitive to certain stimuli.255,256 It is unlike-ly that this sensitivity results from direct stimulation ofnerves in dentin (Figure 2-39). As previously stated,

nerves cannot be shown in peripheral dentin.143,144

Another speculation is that the odontoblastic processmay serve as excitable “nerve endings” that would, inturn, excite nerve fibers shown to exist in deeper dentin,closer to the pulp.143,144,257 The experiments of Andersonand colleagues258 and Brännström259 suggest that neitherodontoblastic processes nor excitable nerves withindentin are responsible for dentin’s sensitivity.

This led Brännström and colleagues to propose the“hydrodynamic theory” of dentin sensitivity, which setsforth that fluid movement through dentinal tubules,moving in either direction, stimulates sensory nerves indentin or pulp.259,260 Further support for the hydrody-namic theory came from electron microscopic exami-nation of animal67,261,262 and human dentin,64,66,67

demonstrating that odontoblastic processes seldomextend more than one-third the distance of the denti-nal tubules. Work by LaFleche and colleagues suggest-ed that the process may retract from the periphery dur-ing extraction or processing.77 Obviously, more inves-tigation will be required before any definitive statementcan be made regarding the distribution of the process.The tubules are filled with dentinal fluid that is similarin composition to interstitial fluid.176

The hydrodynamic theory satisfies numerous exper-imental observations. Although it cannot yet be regard-ed as fact, it has provided and will continue to providea very useful perspective for the design of future exper-iments263–265 (see Figure 2-39).

Effect of Posture on Pulpal Pain. Whenever anappendage is elevated above the heart, gravity acts onblood on the arterial side to reduce the effective pres-sure and, hence, appendage blood flow. This is whyone’s arm rapidly tires when working overhead. Thereduced pressure effect occurs in structures in the headthat, in normal upright posture, are well above theheart. When the patient lies down, however, the gravi-tational effect disappears, and there is a significantincrease in pulp blood pressure and corresponding risein tissue pressure over and above that caused byendogenous mediators of inflammation. In this posi-tion, an irritated and inflamed pulp becomes more sen-sitive to many stimuli and may spontaneously begin tofire a message of pain. This is why patients with pulpi-tis frequently call their dentists after lying down atnight. In the supine position, a higher perfusion pres-sure and, presumably, a higher tissue pressure developin the patient, which cause more pulp pain. Patientsoften discover that they are more comfortable if theyattempt to sleep sitting up, which again emphasizes theeffects of gravity on pulp blood flow.

Figure 2-38 Comparison of pulp tissue pressure with systemicblood pressure in dog. A, Systemic blood pressure, shown on a dif-ferent sensitivity and scale, demonstrates a mean value of about 120mm Hg and a pulse pressure of about 60 mm Hg. B, Pulp tissuepressure taken simultaneously with systemic blood pressure andshown on different scale. Pulp tissue pressure demonstrates a meanvalue of about 30 mm Hg and a pulse pressure of about 10 mm Hg.(Courtesy of Dr. J. G. Weatherred.)

A

B

Another factor contributing to elevated pulp pres-sure on reclining is the effect of posture on the activityof the sympathetic nervous system. When a person isupright, the baroreceptors (the so-called “carotid”sinus), located in the arch of the aorta and the bifurca-tion of the carotid arteries, maintain a relatively highdegree of sympathetic stimulation to organs richlyinnervated by the sympathetic nervous system. Tönderdemonstrated that canine pulps showed large reduc-tions in blood flow when the baroreceptor system wasmanipulated.226 If the human dental pulp is similar, itwould result in slight pulpal vasoconstriction whenev-er a person is standing or sitting upright. Lying downwould reverse the effect with an increase in blood flowand tissue pressure in the pulp. Lying down, then,increases pulp blood flow by removing both the effectsof gravity and the effects of baroreceptor nerves, whichdecrease pulpal vasoconstriction. Thus, the increase inpain from inflamed pulps at night or the transforma-

52 Endodontics

tion of the pain from a dull to a throbbing ache hasrational physiologic bases. The lack of documentationin the literature is owing to a lack of investigation.

Systemic Distribution of Substances from Dentin andPulp. The rate of blood flow115,230,266,267 in the pulp ismoderately high and falls between that of organs of lowperfusion, such as skeletal muscle, and highly perfusedorgans, such as the brain or kidney267 (Figure 2-40). Sincedentinal fluid (the fluid filling the tubules) is in commu-nication with the vasculature of the pulp,240 in theory,substances placed directly on pulp or dentin diffuse to theinterstitial fluid and are quickly absorbed into the blood-stream or into the lymphatics. In vivo evidence indicatesthat both may occur. Numerous authors have demon-strated that substances placed onto dentin or into pulpchambers are absorbed systemically. These substancesinclude radioactive labeled cortisone,268 tetracycline,269

lead,270,271 formocresol,272–275 glutaraldehyde,276,277 andcamphorated monochlorophenol.278

Figure 2-39 Schematic diagram of essen-tials of three theories of dentin sensitivity.A, Classical theory proposed that stimuliapplied to dentin caused direct simulationof nerves in dentin. B, Modified theory pro-posed that stimuli applied to the odonto-blastic process would be transmitted alongthe odontoblast and passed to the sensorynerves via some sort of synapse. C,Hydrodynamic theory proposed that fluidmovement within tubules transmits periph-eral stimuli to highly sensitive pulpalnerves. C more accurately represents theactual length of the odontoblastic processrelative to the tubules. Nerves are seldomfound more than one-third the distancefrom pulp to surface. Modified with per-mission from Torneck CD.90

Figure 2-40 Comparison of blood flowsamong various tissues and organs, adjust-ed according to weight. Pulpal blood flowis intermediate between muscle and heartblood flow. Reproduced with permissionfrom Kim S. J Dent Res 1985;64:590.


This direct communication of dentin to systemic cir-culation was proved by Pashley,184 who demonstratedthat radioactive iodide and albumin placed on dog dentinrapidly gave measurable blood levels of the substances.Systemic absorption of substances following pulp appli-cation was shown by Myers and colleagues, who meas-ured the systemic appearance of 131I from pulpotomysites in monkeys both before and after treatment of thepulp stumps with formocresol.276 Similar studies haverecently been completed using 14C-formaldehyde274,275

and 14C-glutaraldehyde.276,277 Barnes and Langelanddemonstrated that circulating antibodies were formedagainst bovine serum albumin and sheep erythrocytesplaced on exposed pulps of monkeys.120 Thus, the pulpprovides an access route not only to the systemic circula-tion but also to the lymphatic system.106

Noyes and Ladd forced fluid into dog pulps andobserved its collection in submaxillary lymph nodes.279

Kraintz and coworkers placed radioactive colloidal goldon dog dentin and found that it appeared in the lym-phatic drainage.119 Walton and Langeland studied thedistribution of zinc oxide and eugenol from pulpotomysites in monkeys.108 Within days, the particles were dis-tributed throughout the pulp (Figure 2-41) and peri-odontium and appeared in the submandibular lymphnodes of the animals.

Feiglin and Reade deposited radioactive micros-pheres in rat pulps and found more microspheres inthe submandibular lymph nodes in those rats whosepulps had been exposed for 5 days in comparison withthose with acute pulp exposure.280 This suggestsenhanced lymphatic function during inflammation.

The relationship of teeth to the cardiovascular andlymphatic systems is intimate and absolute. Cliniciansshould remember this when performing dental proce-dures since their placement of materials on dentin orpulp may result in widespread distribution of thatmaterial or medicament.

HISTOLOGY OF THE PERIRADICULAR REGION

At the periapex, the connective tissues of root canal,foramen, and periradicular zone form a tissue continu-um that is inseparable. This intimate relationship isconfirmed by the frequency of disease in the pulp,inciting disease beyond the tooth. When both the pulpand periapex are jointly involved, immediate therapymust often focus on the periradicular region. Morecommonly, only pulp therapy is necessary. Healing ofthe periradicular tissue generally occurs spontaneously,demonstrating its capacity to repair. During prepara-tion of the pulp space, the cardinal principles of instru-mentation and obturation, aimed at confining every-

thing to the canal space, indicate how necessary it is torespect the periradicular connective tissue.

The intimate communicative relationship of thestructures at the periapex has been shown in experi-ments that traced substances placed in the coronal pulpto the periodontium. Markers migrated from the pulpand were observed in all areas of the periodontal liga-ment, the alveolar and medullary bone, and even in themarginal gingiva.94,108

The periapex is the apical continuation of the peri-odontal ligament. Actually, the tissue at the immediateapex of the tooth is more akin to the content of the rootcanal than to the periodontal ligament. The concentra-tion of nerves and vessels coursing into the pulp is such,in fact, that attachment fibers and bone normally asso-ciated with the ligament space are generally excluded.The radiographic appearance of the interruption inbone to permit passage of the neurovascular bundlemust not be confused with the bone resorption thataccompanies periradicular inflammation (Figure 2-42).

The connective tissue sheaths of vessel and nervegroups lie close together. It is small wonder that inflam-matory change is found concentrated at this zone ofvessel egress; the spread of inflammation occurs via theconnective tissue sheaths of vessels as a pathway ofspread.113,114

Physiologically, as well as structurally, sharp contrastsset the periodontal ligament apparatus off from pulp tis-sue: (1) It is, for example, an organ of the finest tactilereception. The lightest contact on the tooth will stimu-late its numerous pressor receptors. The pulp containsno such receptors. Proprioceptors of the periodontal lig-ament present the capability of spatial determination. Itis for this reason that an inflamed periodontium can bemore easily localized by the patient than can an inflamedpulp. (2) Collateral blood supply, so lacking within thepulp, is abundant in this area. This rich blood supply isundoubtedly a major factor in the periapex’s ability toresolve inflammatory disease. In contrast, the pulp oftensuccumbs to inflammation because it lacks collateralvessels. (3) The apical periodontium communicates withextensive medullary spaces of alveolar bone. The fluidsof inflammation and resultant pressures apparently dif-fuse through this region more readily than is possible inthe confined pulp space.

Histologically, the periapex demonstrates the majorfeatures of the remaining periodontium. Collagenousfibers anchor cementum to alveolar bundle bone. Thearrangement of bone and fibers is discontinuous wherethe neurovascular bundle passes through to the pulp. Asignificant component of the periodontal ligament at alllevels is the cords of ectodermal cells derived from the

54 Endodontics

Figure 2-41 Experiment in monkeys showing time and spatial pattern of migration of material placed in contact with vitalpulp. A, Human mandibular first and second molars after pulpotomy; application of a silver–zinc oxide–eugenol sealer andrestoration with amalgam. Arrow indicates region shown histologically in B and C. B, Area of pulp canal indicated in A.Particles of silver and zinc oxide are visible in extracellular spaces (E) adjacent to vessels and intracellularly (I) within endothe-lial or perivascular cells. Material is also contained in venules (V) and in small vessels resembling capillaries, or in lymphatics(L). C, Same field as B; polarized light demonstrates particles seen in B, which are birefringent sealer particles. Reproducedwith permission from Walton R and Langeland K.108

B C

A


original root sheath, which form a tight network in thisnarrow zone between tooth and bone. These embryon-ic remnants, the epithelial rests of Malassez, may servein a constructive capacity, and several such functionshave been postulated.281 However, interest has focusedon their potential to undergo rapid hyperplasia whenstimulated by periradicular inflammation. As will beseen in chapter 5, it is these cells that provide the epithe-lial “seed” for the lining sheet of the apical cysts.

Beyond the ligament is the alveolar bone with itsassociated marrow. The transition from ligament spaceto marrow is made through the myriad perforations ofthe alveolar bone proper. This bone, at the periapex asmuch as on the lateral walls of the socket, is truly acribriform plate.122 Interstitial connective tissue of theperiodontal membrane passes through it, carrying ves-sels and nerves, to blend with the fatty marrow of thealveolar-supporting bone.

The potentials of this periradicular marrow are richand significant. The reserve and other cells of the mar-row contribute to nature’s débridement and repair inthe diseased periradicular zone following adequatepulp therapy.

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Ch02: HISTOLOGY AND PHYSIOLOGY OF THE …...Histology and Physiology of the Dental Pulp 27 The human...

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