Remaining dentine thickness and human pulp responses

Remaining dentine thickness and human pulpresponses

P. E. Murray1, A. J. Smith2, L. J.Windsor1 & I. A. Mjo« r31Oral Biology, Indiana University School of Dentistry, Indianapolis, IN, USA; 2Oral Biology, School of Dentistry,The University ofBirmingham, Birmingham, UK; and 3NIOM, Scandinavian Institute of Dental Materials, Oslo, Norway, and College of Dentistry,University of Florida, Gainesville, FL, USA

Abstract

Murray PE, Smith AJ, Windsor LJ, Mjo« r M. Remaining

dentine thickness and human pulp responses. International Endodontic

Journal, 36, 33^43, 2003.

Aim To evaluate pulp responses as a function ofremaining dentine thickness (RDT) of 98 class V cavitypreparations in 49 teeth of 31 patients aged 10^16 years.Methodology Shallow cavities were restored withamalgam, deeper cavities or pulp exposures wererestored with amalgam lined with calcium hydroxideor with zinc oxide eugenol. Teeth were extracted after3^89 days for orthodontic reasons. Following proces-sing for light microscope analysis, the number of odon-toblasts, pulp in£ammation, and repair was recorded.Results In comparison with independent odonto-blasts, the numbers of odontoblasts were reduced by13.6% beneath a RDT of 2.5^0.5 mm, 33.7% beneath

a RDT of 0.5^0.01mm and 99.0% beneath pulp-exposed cavities. Reparative dentine was observedfollowing pulp exposure and reactionary dentine wasobserved with a mean RDT of 0.77 mm (2.5^0.01mm).Reactionary dentine secretion was in£uenced byRDT and restorative materials. Pulp in£ammationwas not in£uenced by RDT in the present study.Conclusions Cavity RDT mediates a powerful in£u-ence on underlying pulp tissue vitality but it has littlee¡ect on reactionary dentine secretion and in£amma-tory activity. Gross tissue injury explains the poor pulpcapping prognosis following exposure and underliesthe need to avoid this type of injury. Following restora-tion, a RDT of 0.5 mm or greater is necessary to avoidevidence of pulp injury.

Keywords: calcium hydroxide, in£ammation, odon-toblast, reparative dentine, zinc oxide eugenol.

Received11February 2002; accepted 29 August 2002

Introduction

The importance of the remaining dentine thickness(RDT) underlying cavity preparations inmodifying pulpresponses to dental materials has been a topic of contro-versy for more than a century (Stanley et al.1975). Overthe years, the estimated value of the minimal cavityRDTwhichdoes not cause pulp injuryhas been decreas-ing. Stanley (1994) suggested that a RDTof 2 mmwouldprotect the pulp from injury caused by most restorativematerials and procedures. Subsequently, Pameijer et al.(1991) reported during luting procedures that a RDT of

1mmor morewould be su⁄cient to protect the pulp tis-sue from the cytotoxic e¡ects of zinc phosphate (ZnP)and resin-modi¢ed glass ionomer (RMGI). Nevertheless,it was recently suggested that restoring deeper cavitypreparations, carefully cut down to 0.5 mm, with zincoxide eugenol (ZOE), intermediate restorative material(IRM) and calcium hydroxide (Ca(OH)2)/amalgam,appeared to have little e¡ect on underlying odontoblastnumbers for up to 381 days following treatment inpatients (Murray et al. 2000b). Moreover, it is unclear ifthe minimum RDT, at which little or no pulp injurycan be observed, varies signi¢cantly between di¡erentpatient variables and restorative materials. An impor-tant source of pulp injury is likely to be the increasedtraumatic operative procedures involved in cuttingdeeper cavity preparations (Stanley 1961, Darvell 1981).

Correspondence: Dr Peter E. Murray, Oral Biology, Indiana UniversitySchool of Dentistry, 1121 West Michigan Street, Indianapolis, Indiana,IN 46202, USA (Tel.: þ1317 2742126; e-mail: [email protected]).

� 2003 Blackwell Publishing Ltd International Endodontic Journal, 36, 33^43, 2003 33

Understanding the interactions between RDT and thedegree of pulp injury may be important in understand-ing why some vital teeth exhibit clinical symptomsleading to the need for endodontic treatment (Zo« llner& Gaengler 2000). Nevertheless, precise information onthe role of the cavity RDT in in£uencing pulpal in-jury and dentinal repair responses with commonrestorative materials is limited (Lee et al. 1992, Murrayet al. 2001).The bu¡ering e¡ect of the cavity RDT to provide pulp

protection can be expected to vary not only with dent-inal tubule distance from the prepared cavity £oor topulp tissue, but also with dentinal tubule permeability.Tubule permeability is an important factor in allowingthe progressionof caries, bacterial leakageand chemicalirritants towards pulp tissue (Mjo« r & Ferrari 2002). Con-sequently, the width of a¡ected tubules and the peritub-ular secretion of dentine in reducing their width tohelp mediate pulp protection are important. Peritubularsecretion takes place throughout life and is most notice-able in the teeth of older patients, and in those that haveexperienced wear/erosion (Mjo« r 2002).In newly erupted teeth, the most pulpal dentine often

has no discernible peritubular dentine lining (Mjo« r1966).Therefore, the permeability and peritubular reac-tion potentials of teeth may be expected to vary withpatient age and treatment history, suggesting thatalthough the RDT between patients can be similar, den-tine permeabilityand pulp reactions may be quite di¡er-ent (Mjo« r et al. 2001). Nevertheless, it is important tocharacterize human pulp responses to RDT followingtreatment to gain an improved understanding of pulp^dentine responses to cavity preparation and restorationvariables.Evidence suggests that reductions in the RDTof cavity

preparations, increasingly make the pulp susceptible totraumatic injuries caused by cavity preparation andrestoration events (Santini & Ivanovic 1996, Murrayet al. 2000a). Thus, it is important to avoid needless den-tine removal during surgery. Nevertheless, often theRDT of cavity preparations will be determined by theextent of disease progression and treatment regime.Accordingly, it is important to quantify thedegreeofpulpinjury in response to a range of cavity RDTs in combina-tion with common restorative materials, such asCa(OH)2/amalgamand ZOE. Few studies have attemptedto quantify pulp injury as a function of RDT, restorationmaterials, or other cavity restoration variables, such ascavity width and cavity wall depth. Nevertheless, mini-mizing pulp injury following treatment and preservingthe numbers of pulpal cell populations, particularly the

odontoblasts, can be critical to maintain function andvitality of the pulp, as well as reducing the probabilityof postoperative complications (About et al. 2001a).Theaims of this studywere to quantify pulp responses

to cavityRDTbymeasuringand correlating patientvari-ables such as age, cavity preparation variables such astooth type, tooth surface of cavity preparation, toothdentine thickness, cavity £oor width and cavity walldepth, aswellas restorationvariables, including the timeelapsed since restoration and type of restoration mate-rial. Pulpal responses were measured using odontoblastand subodontoblast cell numbers, pulpal in£ammation,aswell as dentine bridge and reactionarydentine forma-tion.

Materials and methods

Patient sample and cavity preparation

Thirty-one healthy patients, aged between 10 and16 years of age (mean11.9 years), had 98 classV cavitiesprepared in teeth, which were scheduled for extractionfor orthodontic reasons at the Oslo School Dental Ser-vice, Norway. Patient and parental informed consentwas provided for the teeth to be used for research pur-poses.Atotalof 49noncarious intact ¢rst or secondmax-illary or mandibular premolars were obtained from thearchives of one of the authors (IAM). Cavitypreparationswere cut intoboththebuccal, lingualorocclusal dentineusinga dental hand-piecewithanabundantwater spraycoolant.Teethwere restoredwithamalgam, or amalgamlinedwithCa(OH)2orZOE (Table 1).Teethwereextractedunder local anaesthesia after 3^89 days (mean26 days)observationperiods. Some of these teeth havepreviouslybeen used to study changes in dentine following opera-tive procedures (Mjo« r 1967a,b). All experiments wereundertakenwith theunderstandingand consent of eachsubject.

Histomorphometric analysis

Histological axiobuccolingual tooth sections (5 mm)were prepared through experimental areas of all teeth.Histomorphometric analyses were carried out on hae-matoxylin and eosin-stained sections with an eye piecegraticule �50 magni¢cation. Brie£y, the cavity RDTwas measured as the shortest distance between themid-point of the cavity preparation £oor and the pulpdentine border (Stanley 1968). The cavity wall depth(CWD) was calculated by measuring the distancebetween the cavity £oor and the outermost cut dentine

Human pulp responses Murray et al.

34 International Endodontic Journal, 36, 33^43, 2003 � 2003 Blackwell Publishing Ltd

on both sides of the cavity preparation. These measureswere divided by two, to provide a single mean of thecavity wall depth per cavity preparation (Murray et al.2000a,b,c; 2001, About et al. 2001a).

Reactionary and reparative forms of tertiary dentinesecretion

Reactionary dentine, sometimes called irregular den-tine, was identi¢ed as an area of increased tertiary den-tine secretion with a tubular continuity with thephysiological secondary dentine (Mjo« r1983). The secre-tion of reparative dentine was formed by a new genera-tion of odontoblast-like cells and did not have a tubularcontinuity with the physiological secondary dentine(Smith et al.1995). Adi¡erentiation between reactionaryand reparative dentine was made during the examina-tionof the sections.The dentine at the interface betweenthe primary^secondary dentine continuum and thereparative tertiary dentine has a variable and irregularstructure. It is often atubular as judged by light micro-scopy and it has been referred to as interface dentine(Mjo« r 1983). Dentine bridge is a specialized type ofreparative dentine secretion because it has a tubularcontinuity with the newly di¡erentiated odontoblast-like cells, but not the physiological secondary dentineor reactionary and reparative dentine.

Pulpal in£ammatory activity

Pulpal in£ammatoryactivitywas categorized accordingto de¢ned criteria (Mjo« r & Tronstad 1972, Heyeraaset al. 2001).� No reaction:The tooth pulp contained no or very fewin£ammatory cells, subjacent to the cavity dentinaltubules. All cell strata and predentinewidth appeareduniform and no hyperaemia or haemorrhage wasidenti¢ed. Slight reaction was characterized by anin£uxof small numbers of cells, including small roundlymphocytes, into the cell-free zone in the area adja-cent tothecavitydentinal tubules. Someminor irregu-larities could be observed in the odontoblast layerand predentine thickness.

� Moderate reaction:The odontoblast layerwas present,but partly disrupted by hyperaemia, haemorrhageand polymorphonuclear leucocyte, or mononuclearlymphocyte in¢ltration subjacent to the cavitytubules. The predentine was absent or reduced inwidth.

� Severe reaction:The odontoblast layer was destroyedbylocalised abscess formation, and byan intense in¢l-tration of polynuclear leucocyte lesions extendingfrom the cavity tubules. Hyperaemia was found inthe tissue surrounding the intense cellular in¢ltra-tion. The predentine was reduced in width or absent.

Number of odontoblasts

The numbers of odontoblasts and cells of the subodonto-blast layer were counted per mm at the pulp^dentineborderbeneaththe cutdentinal tubules of the cavitypre-paration. These cell numbers were also counted0.5 mmaway inthree independent positions for compar-ison: immediatelyocclusal to the cavity tubules, immedi-ately apical to the cavity tubules and also directlyopposite the cavity on the adjacent side of the tooth.These cell count locations are shown schematically inFig. 1. The mean from these three areas was calculatedto provide a measure of cell numbers independent ofthe cavity preparation.

Statistical analysis

The raw numerical data was examined using one-wayanalysis of variance (anova) statistics at a con¢dencelevel of 95% (StatView software, SAS Inc., Cary, NC,USA).This statistical procedure is amongst the most ver-satile and conservative of the multiple comparison tests(Dawson-Saunders & Trapp1994).

Results

Remaining dentine thickness of cavity preparations

Pulp responses to cavity preparation and restoration arethe summation of the interplay between these variables

Table 1 Numbers of cavity preparationsexamined according to cavity remainingdentine thickness and restorativematerial

Remaining dentine

thickness (mm) Calcium hydroxide Zinc oxide eugenol Amalgam Total

2.5^0.5 47 17 2 66

0.5^0.01 14 6 2 22

Exposed: 0.01^0.79 8 2 0 10

Total 69 25 4 98

Murray et al. Human pulp responses


as well as patient factors. However, the e¡ects of cavityRDT on individual factors do not appear uniformbecause variations in the degree of correlation betweenRDT and individual factors ranged betweenP ¼ 0.0001and 0.9901. RDTwas not found to be statisti-cally correlated with most of the variables examined(Table 2).

Cavity wall depth

The close similarity between the thickness of dentine inpremolars and the reproduciblepositioningof cavitypre-parations appears to have caused a reciprocal relation-ship between RDT and CWD (Fig. 2). This means thatany proportional increase or decrease in CWD ismatched by an opposite equivalent e¡ect on RDT. Forexample; a lingual CWD of1mm is equivalent to a RDTof 1.04 mm because the addition of both the CWD andRDT always add up to a value of 2.04 mm (�95% con¢-dence interval of 1.817^2.264) (Fig. 2). This suggests themeasurement of CWD may provide a high degree ofaccuracy for estimating cavity RDT, although some var-iations were observed between occlusal, buccal and lin-gual cavity preparations (Fig. 2).

Reactionary and reparative dentine secretion

Dentine bridge formation was highly correlated to RDT(Table 2). This is because the secretion of reparativedentine was observed to take place with a mean pulpexposure depth of �0.15 mm, whilst no reparative den-tine was observed in non-pulp-exposed cavities (Fig. 3).

Figure 1 Schematic representation ofthe cell count locations within teeth.

Table 2 Variables correlated to the remaining dentinethickness of cavity preparations

Variable

Remaining dentine thickness of

cavity preparation (ANOVAP-value)

Cavity wall depth 0.0001

Dentine bridge formation 0.0072

Odontoblast cell numbers 0.0090

Tooth dentine thickness

at site of cavity preparation

0.0650

Age of patient 0.3043

Cell numbers of the

subodontoblast layer

0.6864

First or second premolar type 0.4821

Cavity restorationmaterial 0.7732

Pulpal inflammation 0.8362

Cavity floor width 0.9216

Reactionary dentine area 0.9901



This study can only provide very limited informationbecause 10 pulp exposures were examined and onlythree of these contained any reparative dentine secre-tion. In each case, the dentine bridge deposition wassmall. Reactionary dentine secretion appeared to be amore generalized non-pulp-exposed response with amean RDTof 0.77 mm (Fig. 3); the secretion of reaction-ary dentine did not appear to be signi¢cantly correlatedwith RDT (Table 2). Small quantities of reactionary den-tine were observed in seven from 88 non-pulp-exposedcavities.

Number of odontoblasts and subodontoblast cells

Thenumberof odontoblasts beneathcavity preparationswas highly correlated to the RDT (Table 2). With adecreasing RDT, underlying odontoblast numbersdecreased inanexponentialmanner rather thana linearmanner. Compared with una¡ected odontoblasts, thenumbers were reduced byapproximately13.6% beneatha RDT of 2.5^0.5 mm, 33.7% beneath a RDT of 0.5^0.01mm and 99.0% beneath pulp exposures (Fig. 4).The subjacent subodontoblast cells were less responsiveto reductions inRDT (Table 2); only followingpulp expo-sure, did the subodontoblast numbers decrease by�38.4% (Fig. 4).

Restorative materials and reactionary dentinesecretion

The restorative materials were not found to be di¡erentfrom each other in respect to cavity RDT (Table 2); how-ever, the combination of RDT and restorative materialdid appear to have some e¡ect on reactionary dentinesecretion. Cavity restoration with amalgam alone wasnotassociatedwith reactionarydentine secretion (Fig. 5).ZOE was increasingly associated with reactionary den-tine secretion when the RDT was reduced (Fig. 5). TheRDT did not appear to in£uence reactionary dentinesecretion following restoration with calcium hydroxide(Fig. 5). Information is limited about the e¡ects of

Figure 2 Regression analysis of cavitywall depth and remaining dentinethickness.

Figure 3 Dentine bridge formationand cavity remainingdentine thickness.



reactionary dentine because only seven cases wereobserved from 88 cavities, and the quantity of reaction-ary dentine was small.

Pulpal in£ammation

Little di¡erence was found between the RDTs of none,slightandmoderate categories of in£ammation (Table 2)(Fig. 6).The severe categoryof in£ammation is of limitedusefulness in this study because only one pulp wasassigned to this category.

Discussion

Radiographic plates and endocator equipment can beused to provide estimates of cavity RDT, but thesemeasurements do not re£ect the physiology of dentine.Measurement of dentine tubules along their lengthappears to represent themost logicalandphysiologicallyrelevant method (Langeland & Langeland1966). In thisstudy, RDT was measured as the shortest distance fromthe cavity £oor to the pulp tissue, primarily because ofease of use and avoidance of measuring complications

Figure 4 Odontoblast andsubodontoblast cell numbers withcavity remaining dentine thickness.

Figure 5 Restorative materials andpresence or absence of reactionarydentine secretionwith cavityremaining dentine thickness.



between di¡erent points. The advantage of measuringRDT using this method is that it can be used in conjunc-tion with conventional clinical techniques. Although arelationship probably exists between RDT and tubulelength, especially in deep cavities, there is a clear needto evaluate pulp responses in conjunctionwith dentinaltubule length in future studies. Nevertheless, this studyhas shown how the CWD can be used to estimate RDTbecause of the uniformityof premolar dentine thicknesstogether with careful cavity positioning. In lingual,occlusal and buccal cavities, the maximum dentinedepth of cavity preparation before pulp exposure takesplace was found to be 2.33,1.96 and1.1mm, respectively.Whatever approach is used to estimate the RDTof cavitypreparations prior to their restoration, it is clear thatthe interactions between RDT, cavity preparation andrestorationvariablesare important to theunderstandingof the injuries sustained to the dental pulp, and its capa-city tomediate dentine repair and remainvital through-out life. The basis for a biological approach to clinicalpractice would be to identify and attempt to reducesources of tissue injury, suchasusing thepulp-protectivee¡ect of dentine beneath the cavity £ooraswell as incor-porating the dentine repair capacity of teeth as part oftreatment. Several reaction patterns of dentine repairhave been demonstrated that may be put into clinicaluse directly (Mjo« r 1985, 2002). This requires an under-standing of the pulpal responses to varying cavity RDTsand to the reactivity and reaction patterns of primarydentine.Studies of humanteeth have showna highprevalence

of histological responses to cavity preparation andrestoration events. Dentine bridge formation has been

observed in 90% of teeth following pulp exposure(Baume 1980) and reactionary dentine secretion hasbeen observed beneath more than 50% of restorations(Murray et al.2000a,b). Severe categories of pulp in£am-mation have been associated with low RDTs (Heblinget al.1999). In this present study, only three of10 exposedpulps were associated with dentine bridge secretionand only seven of 88 (8%) non-pulp-exposed cavity pre-parations were associated with reactionary dentinesecretion. A possible explanation for this variation maybe due to di¡erences in the observation periods. Themean observation time was approximately 27 days inthis study versus 46 and 64 days in other studies simi-larly evaluated (Murray et al. 2000a,b). The shorter timeframeof this present studywouldhaveprovided less timefor the dentine repair processes to be fully accomplished.Other explanations for these di¡erences include a varia-tion between patient samples, including the possiblee¡ects of treatment history and other factors such asage. The prevalence and magnitude of pulpal responsescould theoretically be dependent on subjective criteriathatare di⁄cult tomeasure quantitatively, suchasvaria-tions in the healing response between individualpatients and di¡erences in clinical technique betweenclinicians. Little is knownabout the importance of thesefactorsand itwasnotpossible toaddress them inthispre-sent study. Consequently, we have focused on pulp^den-tine responses to RDT or pulp exposure, which issomewhat under the control of the clinician.In an attempt to overcome di⁄culties with the use of

subjective qualitative criteria, quantitative approacheswere used, whenever possible, to assess pulp activityunder controlled conditions of patient age, health and

Figure 6 Pulp in£ammationand cavityremaining dentine thickness.



specimen tissue preparation. This is because qualitativedata always contains an element of subjectivity (Warf-vinge1987). The application of the anovamultiple com-parison test avoided the problem of having to computemany individual comparison tests between histologicalraw data (Qvist & Stotlze1982). If this test were not per-formed, the multiple tests between di¡erent pairs ofmeans would alter the a-level, not for each comparison,but for the experiment as a whole. For example, if thesix pairs of means shown in Fig. 4 are compared usingindividual tests, and if eachcomparison ismadebyusinga ¼ 0.05, there is a 5% chance that eachcomparisonwillfalselybe called signi¢cant, i.e. atype I errorwould occursix di¡erent times. Overall, therefore, there is a 30%chance (6 �5%) of declaring one of the comparisonsincorrectly signi¢cant. The use ofanova by the authorsovercame these problems and in agreement with Daw-son-Saunders & Trapp (1994) provided a versatile andconservative statistical method.Many factors have been suggested to injure the pulp,

including cavity preparation trauma, restorative dentalprocedures, operator hand instrumentation, systemicdiseases, caries, attrition, erosion, chemicals, dentalmaterials and bacterial leakage (Diamond et al. 1966,Baume 1980, Cox et al. 1987; 1992, Magloire et al. 1992,Lesot et al.1994, Smith et al.1994;1995). Often, the factorscorrelated with pulp injury have proved to be controver-sial. Clearly, the RDTor proximity of the injury stimulusto the pulp tissue will have some impact on the severityof pulp response. Often a reduction in proximity of thecavity £oor to the pulp tissue has been reported toincrease reactionary dentine deposition (Murray et al.2000b), whilst other studies have reported little correla-tion between RDT and reactionary dentine activity(Stanley 1961, Santini & Ivanovic 1996). The presentstudy did not demonstrate a relationship between theRDT and the presence of reactionary dentine. This lackof correlation may be related to the minimal nature ofthe responses observed, resulting from the short post-operative extraction schedule. However, the formationof a dentine bridge was correlated to the creation of apulp exposure. This would suggest an accord with pre-vious investigations that cavities prepared close to thepulp tissue can injure the underlying odontoblast cells(Darvell1981, Lee et al.1992). Injury to the odontoblastsmay explain the loss of capacity of these cells to secretereactionary dentine, and the secretion of dentine bridgeby a new generation of odontoblast-like cells (Smithet al.1994).The e¡ect of restorative materials on pulpal activity

has similarly proved to be controversial. Some types

of restorative materials, such as Ca(OH)2-based pro-ducts have been reported to stimulate pulpal repairactivity by increasing reactionary dentine deposition(Stanley 1968), whereas some other studies haveshown the e¡ects of the restorative material on pulpresponses are minimal (Cox 1992). This present studydid not demonstrate a relationship between reactionarydentine secretion and the pure form of Ca(OH)2 mixedwith water as a material liner. This may be due to theprecipitation of crystalline salts within the dentinaltubules, reducing their permeability and preventingany adverse reactions in the pulp (Mjo« r & Ferrari2002).The results fromthis studywerealso inagreementwith previous observations, indicating the negativee¡ect of ZOE (Stanley 1968, Kirk & Meyer 1992) andamalgam on reactionary dentine secretion. A smallerRDT was required to observe reactionary dentine withZOE and no reactionary dentine was associated withamalgam, although amalgam was only used to restorevery shallow cavity preparations. Therefore, the largerRDT may be responsible for the lack of reactionary den-tine, rather than the chemical activity of amalgam,because reactionary dentine activity is reduced withincreasing RDT (Stanley et al. 1966). The therapeuticsigni¢cance of why some restorative materials may beassociated with larger areas of reactionary dentine isdi⁄cult to explain because of the limited informationavailable.However, changes in the bu¡ering e¡ect of dentine

with di¡erent RDTs can in£uence the cytotoxicity andchemical activity of restorative materials on underlyingpulp tissue (Murray et al. 2000c). Alterations in dentinephysiology and chemistry in di¡ering tooth locationsmay also be able to explain some di¡erences. For exam-ple, Ca(OH)2 on primary dentine will quickly cause pre-cipitation of mineral salts within the tubules (Mjo« r et al.1961, Mjo« r & Furseth1968) and that will reduce dentinepermeability and in£uence pulp tissue reactions. Thisbiologically positive e¡ect can be used to prevent reac-tions from restorative materials when Ca(OH)2 is usedas a liner (Mjo« r1963).Some areas of coronal dentine showmarked variation

in the structure of the tubules, e.g. the tubules in themost pulpal dentine in newly erupted teeth have nodiscernible peritubular dentine lining themwhilst thosein thebulkof dentine are relatively uniformandare linedby peritubular dentine (Mjo« r 1966). The structure andreaction potentials of this dentine will vary dependingon the age of the patient and wear/attrition amongstother factors that may have a¡ected the tissue. In teethfrom young individuals, the dentine will be truly



una¡ected and therefore more permeable than thedentine in the central part of the cavity preparation,which may have mineralized due to caries. This situa-tion calls for particular attention to the protection ofthe most peripheral part of cavity preparations, and oflarge parts of crown preparations, especially those onintact teeth of young individuals (BjMrndal & Mjo« r2001).Cavity positioning is also important because the area

of tubules exposed by the preparation can vary fromabout 80% of the total area in deep preparations in teethfromyoung individuals to 4% in preparations in the per-ipheral part of the dentine in teeth from individuals inanyagegroup (Ketterl1961). Consequently, the bu¡eringe¡ect of dentine tubule structure in preventing theprogression of caries, leakage of bacteria and penetra-tion of chemicals, appears to be just as important asthe RDT in providing pulp protection (Mjo« r & Ferrari2002).The combined e¡ects of bacteria and their toxins has

been strongly associated with increased pulpal in£am-matory activity. This in£ammatory activity has beenassociated with injury to pulpal tissue and reductionsin the numbers of vital cell populations (Bra¤ nnstrom1984, About et al. 2001b). The absence of bacteria at thecavity margins in this present study probably explainsthe lackof pulpal in£ammatory reactions and the failureto identify any signi¢cant correlation between cavityRDTand pulpal in£ammation.This suggests that pulpalin£ammation is not primarily stimulated by the e¡ectsof cavity preparation followed by restoration withCa(OH)2, amalgamor ZOE.However, the RDTof prepara-tions may be critical in modifying pulpal responses tomore injurious restorative materials, such as adhesives(Hebling et al. 1999) and also in the presence of cariesand bacteria.This study has provided evidence to highlight the

complex interplay between restorative materials, cavityRDTand cavity dimensions which can interact togetherto injure the pulp tissue. Clearly, cavity RDT plays a cen-tral role in determining the extent of pulpal injury andrepair responses.Themechanisms involved in the detec-tion of dentine damage, its transduction to the odonto-blasts and the stimulation of increased odontoblastdentine synthesis and secretion remain incompletelyunderstood (Kardos et al. 1998). However, damage tothe odontoblastic process, injury to the intratubular ele-ments, nerve damageand thepresenceof bioactivemole-cules solubilized from the injured dentine matrix, maybe involved (Smith etal.2001).Currently, followingcavityrestoration, a high proportion of teeth with vital pulps

exhibit symptoms requiring endodontic treatment (Zo« ll-ner & Gaengler 2000). Although the mechanisms ofodontoblast peritubular and tertiary dentine secretionremain incompletely understood, the ability to antici-pateandmanipulate itsactivityshould formpartof treat-ment planning. The basis for a biological approach toclinical practice would be to identify and attempt toreduce sources of tissue injury, and also exploit the den-tine repair capacityof teeth intentionallyas part of treat-ment. This should help to minimize postoperativecomplications following restorative treatment. Animproved understanding of the degree of pulp responsesto varying RDTs will help with the identi¢cation of pul-pal complications.

Conclusion

ARDTofmorethan0.5 mmisnecessary toavoidcausingany evidence of pulp injury. These observations high-light the importanceofmaximizing theRDT to limitpulptissue destruction.Restorative treatment is possible evenif pulp injury is disregarded; however, if restorative den-tistry is to evolve as biological science, this injury mustreceive attention, clinically as well as in continuedresearch e¡orts. The gross tissue injury created by pulpexposure explains the poor prognosis of direct pulpcapping and underlies the need to avoid this type ofinjury.

Acknowledgements

This work was supported in part by grant no. 057820from theWellcome ResearchTrust Foundation.

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Remaining dentine thickness and human pulp responses