Pulp Dentin Biology(1)

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Pulp-dentin biology in restorative dentistry.Part 4: Dentai cariesCiiaracteristics of iesionsand puipai reactionsLars B jrndal, DDS, PhDVIvar A, Mjr, BSD, MSD, MD, DrOdont^

The infectious disease dental caries resuifs in lesions thai may affect enamel, dentin, puip, and cementum.If a caries lesion has progressed to the stage at which it requires restorative intervention, it is importantthat the ciinician un derstand the tissue chang es in the dentin that are iikeiy to have taken place during le-sion de velopme nt. Until the present, no m ajor distinction between the restorative treatment of active(rapldiy progressing ] a nd arrested (slowly progressing) lesions has been m ade, despite the faot that thetwo conditions exhibit major differences in tissue change s in the puip-dentin complex. Intralubuiar chan gesand tertiary dentin formation will affect the outcom e of the restorative treatment. In unaffected dentir andin rapidly progressing lesions, permeabie tubules persist, and when the preparation of carious teeth re-sults in the open ing of unaffected d entin, greater care must be taken in ali phases of the restorative proce-dures tha n if the dentin is imperm eable. An active, deep iesion can be changed to an arrested lesion by atwo-step excavation approach. Optimal assessment ot the prevailing ciinical conditions can only be madeon the basis of thorough knowledge of the biology of the pulp-dentin organ. (Quintessence Int 2001:32:717-736)Key words: caries lesion, demineralization, dentin, enamel, odontoblasts, pulp, remineraiization, stepwiseexcavation, tertiary dentin

he infectious disease dental caries results in lesionsthat affect enamel, dentin, and pulp, and cemen-um if the root portion of the tooth is involved. Theselesions will be referred to as caries lesions. They areharacterized by demineralization of the hard tissuesf the tooth, accompanied by tissue changes in the af-ected primary dentin and inflammatory reactions inhe puip.ITie reasons for dental restorative treatments differ,dual treatment. When preventive, nonopera-

rofessor, Departm ent of Cafiology a nd Endodontics, School ofDen t is t ry , Facu l t y o f Hea l th Sc iences , Unrve rs i t y o f Copenhagen ,Copenhagen, Denmark.Dentistry, University of Florida, College ot Dentistry, Gainesuille, Florida;NIOM, Scandinavian institute ct Dental M atenais, Hasium, Non^ay.

t r e q u e s t s : D r L a rs B j a rn d a i , D e p a i tme n f o t C a r i o l o g y a n d

his is one ot seven articles in a series emphasizing a blologio approach toestorative dentistry through an understanding of file pulp-dentin compiex.

sound, unaffected dentin. Intact teeth may likewise heused as abutment teeth for fixed partial dentures.Furthermore, restorations are frequently replaced be-cause of failure and sometimes because of cosmetic de-mands made by the patient. ' The conditions forrestorative therapy are, therefore, quite different fromtooth to tooth, not only as a result of variable pathosesand associated tissue changes, including age-relatedchanges, but also because of variations in the size andactivity of the individual caries lesion. To optimize theprofession's understanding of these differences, the pre-sent review will focus on the gradual development fromearly enamel lesions to deep dentin involvement andthe associated ptilpal reactions.The development of caries lesions is not a one-wayprocess of demineralization, but an intermittentcourse of demineralization interspersed with mineraluptake or remineraliiation,^'^ The key factor in the de-velopment of caries lesions is the presence of micro-bial, acid-producing plaque on the surface of tbetooth. The metabolism of the plaque varies dependingon many factors, including dietary intake and oral hy-giene, which explains the cycle of demineralizationand remineraiization. A progressing lesion is referredto as an active lesion. In the enamel, it has a dull

white, opaque appearance (Pig 1). In the dentin, a softyellowish or light to dark brown discoloration of thedemineralized tissue prevails (Fig 2).


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Fig 1 Active primary enamei iesion represented by a wbiie, auiimesiai surface on a mandibular first moiar The lesion has beenmade isible tollowing exfoiiation of tbe primary second molarFig 2 Yeilow emineraiized denlin in an aoliue, progressinsion, made visible iolioming the removai of undermined enamthe maxiiiary lirst premolar. No denlin has yet been excavand a gentle touch with an explorer reveis penetration and ening of a fragment of demineraiized tissue

Fig 3 Arrested approxima i iesion on a mand ibular molar withcavitation iocated in the enamel. Tine surfaoe is shiny and discol-ored. The adjacent too tii has been e xtracted; the resuitant changein the cariogenic environmenf has allowed the lesion to becomearrested.

Fig 4 Expose d, siowiy progressing iesion in a maxiilary prlar The demineraiized dentin has a dark appearance. The cent tooth has been extracted, causing a change in the cgenic environment. As a result, the iesion has bec ome inactior arrested.

Fig 5 Secondary caries in a second moiar. deveioping g ingivaiiyadjacent fo fhe resforation. Apart from its location, it is basicaily

The process may be permanently stalled undevorable conditions, a condition referred to as arrcaries. Depending on the extent of the injury prodby the caries, arrested lesions will have a varied appance, ranging from a shiny, white, opaque or discolspot in the enamel (Fig 3) to a hard, dark dentinal face exposed to the oral environment (Fig 4),

Different types of caries lesions have heenscribed; primary, secondary (rcurrent), and remlesions. This article will focus on primary lesCoronal caries starts on intact tooth surfaces, andearly enamei lesion will be described to the extenquired to understand the reactions in the dentinpulp. Secondary lesions, often referred to as seconcaries, develop adjacent to restorations. Apart f


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Bjarndai/Mjr (Lett) Ground section of a subsur-

(Original mag nil cat on x3 0.)(Rigi^t) Microradiograph of an un-

oot surlace canes lsion. The subsurfaceesion phenomenon is shown in cementum.ote the increased mineraiization in theentin subjacent to the iesion. {Originalagnification x3.)

hey are basically similar to primary lesions^'^ and willot be discussed separately in this article. Remainingcaries represents part of the caries lesion left behind inhe preparation or at the enamel margin of a prepara-ion when a restoration is placed.

PRIMARY ENAMEL LESIONShe classic description of the morphogenesis of therimary enamel lesions starts with the so-calledhite-spot lesion, defined as the first macroscopicign of caries-induced demineralization^ (Fig 1).hen a white-spot lesion is viewed histologically, anpparently well-mineralized surface zone is seen over-

Fig 6), experimentally exposed coronal dentin,' or

More than 50 years ago, the mterpretation of the

the subsurface lesion. Scanning electron microscopyhas shown that the surface layer is not intact but has asurface dissolution pattern with widened intercrys-talline spaces, which explains the dull clinical appear-ance of active lesions.'6 Moreover, arrested lesionsshow no specific evidence of reprecipitated "repair"crystals in the surface layer.'' On the other hand, signsof wear may be noted, which explains the shiny sur-face found on some arrested enamel lesions.Because the chemical dynamics of the developmentof natural enamel lesions involve ongoing sequencesof mineral dissolution and uptake, remineralizationbecomes an integral component in the understandingof the structural characteristics of the caries lesion.Eurthermore, it is important to understand that theremineralization cannot act as an isolated repairmechanism. Mineral uptake from saliva, including ad-ditional fluoride from enamel or topically applied fluo-ride, is a contributing factor in tbe development of tbestructural appearance of the lesion.Although the composition of surface enamel issomewhat different from that of the subjacent enamel,including a relatively bigb fluoride con tent, it is impor-tant to note that, if the surfaee enamel is removed, asubsurface lesion will still develop.'^''^ Thus, the spe-cial characteristics of surface enamel are properties ac-quired as a result of exposure to the oral environment.The organic pellicle, about 1 pm thick, covers all intraoral surfaces, including the hard tissues. It plays asignificant role in the development of subsurface le-sions. The pellicle is the substrate on whicb bacteriawill attach and form plaque. If the pellicle is removed,


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eg, by polishing witb pumice or by grinding, it willstart to re-form quickly in vivo (in minutes rather tbanhours) because of adsorption of proteins from thesaliva.However, because subsurface lesions can be in-duced in vitro,i'''2 tbe presence of a peilicle is not es-sential for tbeir development. M ueb researcb bas beendone on artificially initiated lesions, especially in rela-tion to factors that affect the remineralization of le-sions. An intraoral cariogenicity test using hovineenamel bas also been developed.^' Tbe artificially in-duced lesions do simulate the subsurface characteris-tics of enamel lesions, but tbese lesions are demineral-izations and not true caries lesions. Tbe clinicalrelevance of tbe results obtained must, tberefore, beinterpreted cautiously.A series of bistologic and ultrastructural cbangesoccur in vivo during tbe initiation of active enamelcaries lesions before tbe well-recognized signs of awbite-spot lesion can be discerned.22 Tbere is a closerelationsbip between tbe activity of a time-controlledmicrobial, acid-producing plaque and tbe degree ofdemineralization. As the demineralization deepens,the area of the surface zone also increases. Similarly,quantitative analysis of natural approximal lesions^^shows that the greatest degree of tissue porosity al-ways follows the direction of the enamel rods from thedeepest point of penetration to the surface. Mea-surements of the thickness of tbe surface zone indicatethat it increases with lesion progression. The thicknessof the central part of the surface zone is typicallygreater than that observed in tbe peripberal part of thesame lesion, indicating that the surface zone and thesubsurface demineralization are closely correlated toeach other (see Fig 6).The early caries lesion on approximal surfaces takeson a conical sbape, wbich projects into a triangularshape in a two-dimensional ground section wbenviewed in reflected light (Fig 8). If allowed to progress,the lesion will reach the dentinoenamel junction [Fig9) and continue into the dentin (Fig 10}. In all areas,the lesion advanees in a direction parallel to theenamel rods, and the depth of demineralization willvary depending on the time each rod has been sub-jected to tbe caries at tack." Although tbe lesionevolves as a unit. Its particular shape may be best un-derstood if eacb enamei rod is envisioned as develop-ing individually, as a "minilesion.''^" The oldest, deep-est part is located in the center and the youngest,shallowest part is at the periphery. In tbis way, theconical sbape of the enam el lesion is estahlished.

The practical implication of this pattern of develop-ment is that the peripheral extent of tbe subsurfaceenamel lesion always represents the total area of the

However, the depth of demineralization for eminilesion, ie, the individual rod lesion, is c'iffcitntthat the oldest, central part is the most ^idvanThus, when projected along the enamel rod:., the textent of the lesion is similar toward the dentenamel junetion as it is toward the outer imlaceany given time. However, the depth of deniineraltion varies (Fig 10). Consequently, the effect on dentin is less marked at the periphery than it is atcentral part of the lesion.

Tbe conical shape of the advancing enamel lesiobest illustrated on smooth surfaces, eg, on approxisurfaces just below tbe contact points wbere lesusually start (Fig 8).^' Tbe anatomic configurationtbe enamel on occlusal surfaces with tbe groove-fosystem, including pits and fissures, makes it somewdifficult to follow tbe direction of the rods. Lesialso develop baek to back as it were, on the two wof a groove, or at the entrance of a fissure.^^ As tadvance and finally merge at the dentinoenamel jution, tbe actual origin on the surfaee is sometimhard to establish. Thus, early occlusal lesions maydifficult to discern clinically, but tbey can be detecafter careful cleaning and air drying of grooves andsures, and tbey can be treated successfully witb novasive techniques.25,37

ENAMEL-DENTIN LESIONSReviews of the histopatbology of carles have typicfocused on either early stages in the enamel^ or vanced lesions witb bacterial invasion and destrucof dentin.2s Clinically, tbe terms enamel cariesdentinal caries bave been interpreted as two indedent entities. However, effects on dentin may alrebe seen at early stages of enamel lesions (Fig 8), pto surface breakdown and bacterial invasion.Histoiogic evidence shows that the first alterain dentin is a hypermineralized zone that develeven before tbe enamel lesion reaches the dentenamel junction.25.M Subsequent demineralizationtbe dentin is initiated when the enamel lesion reacthe dentinoenamel juncfion. It appears tbat tbe indemineralization never takes place in sound debut is actually a demineralization of affected bymineralized tissue and corresponds to the deepest of tbe enam el rods affected by the caries, ie, tbalong the central part of the lesion (Fig 9), As thesion progresses, the involvement of dentin becogreater (Figs 10 and 11),

The dentin demineralization and the dentin hymineralization never exeeed the area correspondinthe limits of tbe outer enamel lesion; ie, they do


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B0rndal/Mjor Figs 8 to 11 Ground sections through the central part ot tour progressive stages ol approxi-mai enamei iesions i'lewed in reliected iigiit (Originai magmtication y2 5.)

Fig 8 Note the trianguiar shape ot theenamei lesion before il oontacts ttie denti-noenamei junction and ttie subjacent initialhypermineralizaticn ct the dentin.Fig 9 When ttie enamel lesion oontactsthe af tected dent in, more pronounceddentin changes are fcun d. but they are lim-iled in extent to those in the enamel lesion.

Fig 10 As Ihe lesion progresses further,the extent of the dentinal lesion corre-sponds to that of the peripheral enamel le-sion.

Fig 11 When enamei cavitation oocurs,similar relationships prevail between the ex-tent of the enamei iesion and the subjacentreaoticns in dentin The extent of the darkbrownish discoloration of the dem ineraiizcddentin is limited to the surtace area ofenamei rods affected by the caries iesion.


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lesion. However, as indicated in the discussion of thedevelopment of the enamel lesion, not all rods are af-fected at the same time and, therefore, to the same ex-tent. Thus, the reactions of dentin reflect the changesoccurring in enamel, giving rise to two principal alter-ations in the dentin tissue; First, when demineraliza-tion involving groups of rod and inter-rod enamel ap-proaches the inner third of the enamel and progressestoward the dentinoenamei unction, tnineral alterationscan be detected intratubularly in the dentin. Second,when demineralization of enamel reaches the denti-noenamel junction, demineralization uf the dentinstarts, and some of the dissolved minerals will repre-cipitate following the pH-dependent gradients withinthe enamel lesion. In general, the youtigest part of thelesion is found peripherally, both in enamel and dentin.This particular reaction pattern has resulted in thenotion that there is a laterai spread of caries lesions althe dentinoenamel junction, based largely on the clini-cal and radiographie appearance of approximal ie-sions. This concept of the spread of caries lesions isaccentuated because the mantle dentin normally has arelatively lower degree of mineralization at the denti-noenamel junction than in the bulk of the coronal cir-cumpulpal dentin. f*However, at precavitated stages ofcaries, the lesions follow the hasic rules of dentinaipermeability, demonstrating that the primary dentinaitubules are the most significant routes for solute diffu-sion through the dentin.^iThe belief that caries lesions spread at the denti-noenamel junction has led to the conviction that cav-ity preparations must be completed beyond the extentof even preeavitated enamel lesions in order to elimi-nate undermined enamel prior to restoration, but theouter periphery of the enamel lesion actually deter-mines the extent of the dentin lesion.'' No true "lat-eral spread" of the lesion occurs as it reaches thedentinoenamel junction, and consequently no soundenamel is undermined during precavitated stages ofenamel lesion progression. Even eavitation restrictedto the enamel shows the same type of enamel-dentinlesion appearance, in which there is no uncontrolledspreading pattern (see Fig 11). In addition, recentquantitative histologie evidence has shown that theprogress of occiusal enamel lesions at the dentino-enamel junction is basically similar to that of lesionson flat surfaces,^-

Slowly progressing lesionsIn slowly progressing caries lesions, increased miner-alization of the subjacent dentin is normal (see Fig 7).This is a typical reaction in primary dentin to a mildor moderate external stimuli of any sort. In addition to

, ^ ' ' tertiary dentinogenesis will take pl;"* jacent to the affected dentin. ^ The structu re of thetiary dentin can be related to the activity of the lesin that the more active the lesion, the more irregthe structure of the tertiary dentin.^'' This variatiostructure may also be related to reactionary and reative variants of tertiary dentin,*"The initial changes in primary dentin involve setion of the highly mineralized peritubular dentin reduces the diameter of the tubules. This secretakes place pr ior to dent inai deminera l iza tIntratubular mineral deposits within the demineized dentin may also obturate the tubules. Theseposits represent reprecipitations o some of the mials dissolved by the acids that have caused the leto develop. They are significant defense mechanibecause they reduce the permeability of the denwhich in turn reduces the opportunities for ingresbacterial antigens and agents that may cause inflmatory reactions in the pulp.'"-'^The permeability of dentin subjaeent to cariessions in teeth from individuals 20 to 28 years of was only 14% of that in unaffected den tin in indivals from the same age group."^ In the 45- to 69-age group, all dentinai samples subjaeent to cariessions were impermeable according to the methused. Deposition of intratubular mineral crystals shown in the affected dentin. Similar mineral depoin the tubules subjacent to caries lesions in dehave been shown to be composed of hydroxyapaand whitoekite crystals.-*^

The positive effect of intratubular precipitationmineral crystals as a defense mechanism must be phasized. They are reprecipitated during sequencevarying pH gradients in the lesion. In slowly progring lesions, these changes are pronounced becausedemineralization is not aggressive. The intratubcrystals per se do not actually cause the arrest oflesion. Instead they should be considered to be a csequence of the caries activity and a positive effecpreventive measures such as removal of the microbacid-producing plaque covering the lesion.

The application of individually based prevenmeasures, including professional plaque removal, shown that lesions can be successfully arrested,'caries still develops under these conditions, sloprogressing lesions are the most common outcompopulations with an adequate exposure to fluorideg, through the use of fluoridated toothpaste twdaily. If no additional preventive treatment is ployed, lesions in permanent teeth may take 5 tyears to develop to a stage that requires removadamaged tissues followed by the placement of resttions. These lesions tend to remain without clin


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Rapidiy progressing lesionsRampant caries, coupled with inadequate oral hygienend inadequate exposure to fluoride, results in activend rapidly progressing lesions, botb in enamel anddentin. Tbe dentinal reactions associated witb slowlyprogressing caries do not prevail to tbe same extent.Breakdown of the affected enamel and dentin wiiloccur in months, rather than years, and will result inchanges in tbe odo ntohlast-preden tin region, inciudingdestruction of the odontohlasts and lack of formationof tertiary dentin.The subjacent pulpal tissue will react to the trans-mission of microhial products through a permeabledentin hy releasing or activating mediators from poly-morphonuclear and mononuclear leuiiocytes, includ-ing lymphocytes and macrophages or blood plasma.These reactions will initiate the complex inflammatoryevents leading to either reversible or irreversihle stagesof pulpitis, which may or may not he associated withsensitivity or p ain.If tbe odontoblasts are destroyed, tertiary dentinwill form under favorable conditions. Tbis bard tissue,especially that formed initially, is often atubular andmay have cellular inclusions, deflned as fibrodentin'^or interface dentin.-*'^ The healing process will be en-hanced if the cariogenic environment is removed oraltered, and the seq uence may then be followed by thedifferentiation of new, secondary odontoblast-likecells that lay down new tubular matrix, also defined asreparative dentin.^" If, however, the lesion is allowedto progress, the pu lp m ay become infected and perm a-nently damaged, requiring endodontic treatment priorto restoration.

PULPAL REACTIONSxtensive research has been published on pulpal reac-ions in teeth subjected to caries.^i-" Much emphasisas been placed on the correlation of clinical symp-ow classification of the degree of pulpitis for use in

As time progressed, the criteria for evaluation

patients, were often not considered. These limitationsin information make it difflcult to assess the data. Asummary of pulpal and dentinal reactions to caries,based mainly on demineraiized sections from a largenumber of teeth, has been published.^'It is difflcult, and somewbat clinically irrelevant, tobase discussions of the caries-related histopathology ofthe pulp on stained, demineraiized sections uniess de-tailed, chronologic knowledge of the changes in tbedentin and the rate of progression of the lesions hasbeen developed.Despite all the uncontrolled factors in reports ofpulpal reactions to caries, some broad conclusionscan he drawn; The pulp subjacent to deep caries le-sions sbows tbe presence of cbronic inflammatory ex-udate, including lymphocytes, macrophages, andplasma cells.^w.^" Formation of tertiary dentin usuallytakes place on the pulpal aspect of the affectedtubules. The localized increase in dentin thickness isoften accompanied by a reduced odontoblastic layerin the aflected area.The depth of hacterial penetration into the dentinhas been claimed to be decisive for the degree of in-flammatory reaction, and, whenever the bacteria reachthe tertiary dentin, severe pulpitis prevails."^"'^' Thepulpal reactions are well delimited and localized tothe aflected dentin. In tbis respect, histopathologically,the pulpal lesions correspond to the houndaries of thelocally increased tissue fluid pressure associated withpulpal inflammation.^^ The importance of neurogenicinvolvement in pulpal reactions to caries has also beendemonstrated.^' Growth factors present in the deniinare also released during demineralization.S'' They maybe important in tbe initiation of defense mechanismssuch as formation of tertiary dentin.^^The onset of pulpal reactions to caries has been re-ported to occur early, but the phenomenon has beendifficuft to study because th e enamel is lost when tb esections are prepared for routine histopatbologic ex-amination of the dentin and pulp. The relationship tothe lesion is then lost. The localization of noncavitatedand cavitated approximai enamel lesions has beenstudied in newly erupted teeth after grooves were pre-pared through the enamel into dentin in areas not af-fected by caries.52 This approach allowed location ofthe site of the lesion and aided in estabhshing the di-rection of the histologie sectioning. The affectedenamel with the lesion in situ was dissected free fromthe dentin prior to the demineralization required forroutine histologie sectioning. Undemineralized sec-tions were then prepared from these pieces of enamelfor microradiographic examination. Thus, the degreeof ceiiuiar infiltration and tertiary dentin formationcould he correlated to the extent of the enamel lesionwith a fair degree of accuracy.


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Pulpal changes were found subjacent to enamel le-sions without cavitation in 50 of 74 teeth. In 33 of theteeth with pulpal reactions, the caries lesions werelimited to the enamel. Pulpal reactions were evennoted subjacent to shallow white-spot lesions.^^Problems associated with studies of pulpal reac-tions to caries, such as the use of demineralized teeth,direction of sectioning, location of the lesion after sec-tioning, caries activity of the lesion, and the age of thepatients, have already been mentioned. In add ition, noor only Hmited cbaracterization of the tissue changesin the dentin has been undertaken in routine pulpalstudies, either clinically or histopathologically in rela-tion to the mineral content of the dentin. Significanttissue changes in the primary dentin, such as obtura-tion of the tubules and the resulting reduced dentinpermeability, have largely been disregarded.

The reason that undemineralized and demineral-ized sections are not studied at the same time ismainly because of the difficulties involved in studyingthe organic and the inorganic phases of the tissues intheir normal relationship, ie, in the undemineralizedstate. The den tin w ill be m arkedly different in rapidlyprogressing or "acute" lesions than it will in arrestedor "chronic" lesions. This technical problem in prepar-ing sections of teeth for light microscopy can be over-come,^^'^^ but the loss of tissue during the preparationof the sections represents a major problem for detailedanalyses of the entire tooth.With this reservation, the use of undemineralizedtooth sections of the central, and therefore most ad-vanced, part of a caries lesion makes it possible to ob-tain overview sections showing concomitant cbangeswithin the enamel, dentin, and the corresponding pulp(Eigs 12 to 15). Such a technique was used to carefullyexamine and histologically classify 36 clinically well-defined enamel caries lesions without cavitation,based on increasing depths of the lesions.^ 'Computerized histomorphometric analysis revealedthat th e involved odontobiasts in active enamel lesions

reaching the dentinoenamel junction were signifi-cantly smaller than were odontobiasts at tbe controlsite. No significant changes in the size of odontobiastswere noted subjacent to arrested lesions of similardepths. In addition, cellular proliferation in the cell-free zone was noted, whereas this was not observed inarrested lesions. Thus, the odontobiasts and subodon-tobiastic cells are activated early in the progress of thecaries lesion, just as they react rapidly to the removalof cariogenic plaque.3' Changes in the subodontobias-tic region also occur early, and these changes mightinclude the eariy onset of neurogenic inflammatory re-actions (Figs 16 and 17).

The chronology of the initiation of the odontoblas-

with any degree of certainty. However, wlien unmineralized sections are examined, the first indtions of cellular reactions (Fig 18) are noted in aclesions involving more than a quarter of the thickof the enamel.3' These active lesions do not show discernible alterations in dentin mineralization 19). Concom itantly with the formation of hyp^ rmialized dentin, the homogeneity of the predentin be altered, and a change in the organization of the lagen fibrils prevails (Eig20). Diagrams of these stare shown in Eigs 21 and 22 .As soon as the noncavitated enamel lesion cadem ineralization of the affected den tin, evidenctertiary dentin may be noted at the pulp-dentin borinvolving the primary odontobiasts, also deflned aactionary dentin^^ (Fig 23). Eventually these cellslost and the number of tubular structures decreasethe tertiary dentin {Fig 24), The adjacent cells arbroblast-like, with nonpolarized nuclei, and atubtertiary dentin is laid down (Fig 25). In contrast,tertiary dentin in slowly progressing lesions resemthat of tbe physiologic secondary dentin (Fig 26). dentin has the potential for normal tissue changes result of mild to moderate stimulation from chrcaries lesions. As previously illustrated, this can place where an adjacent tooth has been extracted Figs 3 and 4) or in areas where growth conditionsthe microbial ecosystem are reduced. Eigures 27 toshow the principal changes during stages of sloprogressing caries.During the last 20 years, much emphasis has bplaced on the permeability of the dentin in the assment of pulp-dentin reactions,^ with good reaThe initial ports of entry to the pulp for bacteria, terial antigens, toxic, and allergenic componentsthe dentinal tubules. Therefore, studies are needeevaluate both the inorganic and the organic phasedentin in the same sample to correlate with caries restorative procedures.

Furthermore, studies of the immune system ofpulp have clarified some of the defense mechanismthe pulp. Specifically, in relation to carious dentincreased accumulation of immunocompetent cellsbeen demonstrated in the pulpal tissue, as showFigs 21 and 22.^^ Attention has been paid to the dritic cells of the pulp. They are present alongodontoblastic layer even before the onset of exteinjuries, Therefore, immunocompetent cells areportant during the initial exposure of antigens topulp.'i These cells have not been observed follothe formation of tertiary dentin.'^

The importance of interactions among immcompetent cells, release of neurogenic peptides,vascular changes related to caries and restorative


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Bjarndal/MjiFigs 12 to 15 Central part ol an occlusal lesion on a biseoted loolh. (Originalmagnificalton x 5 From B|0rndal et al.3' Reprinted with permission.^

Fig 12 Photograph of the lesion be- Fig 13 Thm, undem ineralized sec-fore tfiin sectiOhs were prep ared . (ion viewed in tfie light microsoope.

Fig 14 Thin, undemineralized sec-l ion v iewed microradiographical lyThe dentin demineraiization (DD] isrestricted to the oontact area of theenamel lesion (HD] Hyper mi ne rail zeddentin.

Fig 15 Example of lesioh (X] andcontrol () areas. The hyperminerai-ized dentin appears diffrent, de-pending on the microscopic lech-nique employed. Note the differencein appearanoes of Ifie lesion and un-affected controi areas, and comparethose appearances fc those shownwith (he microradiographic technique(Fig 13) and another i ight micro-scopic technique (Fig 14).


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Pulp Dentin Biology(1)