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J Am Dent Assoc, Vol 131, No 3, 321-329.
© 2000 American Dental Association
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RESEARCH

POSTOPERATIVE PULPAL AND REPAIR RESPONSES



PETER E. MURRAY, B.SC. (HONS), IMAD ABOUT, B.SC., PH.D., PHILIP J. LUMLEY, PH.D., M.DENT.SC., B.D.S., F.D.S.R.C.P.S., GAY SMITH, B.SC., M.SC., JEAN C. FRANQUIN, B.SC., PH.D. and ANTHONY J. SMITH, BS.C., PH.D.


   ABSTRACT
TOP
 ABSTRACT
SUBJECTS, MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Background. Each year in the United States, the success of 10 million surgically restored carious lesions depends on a favorable tertiary dentin repair response to preparation, restoration and patient factor variables. The authors investigated the relationship between these variables and dentinal response.

Methods. Standardized rectangular Class V restoration preparations were cut into the buccal dentin of intact first or second premolars of 27 patients without exposing the pulp and were restored. The patients were between 9 and 17 years of age. The treated teeth were scheduled for extraction for orthodontic reasons. After tooth extraction, the tertiary dentin was analyzed histomorphometrically.

Results. The area of tertiary reactionary dentin was found to be correlated using linear regression analysis of variance with restoration residual dentin thickness (P = .0024), age of the patient (P = .0045), restoration floor surface area (P = .0266) and restoration width (P = .0415). The authors did not find a correlation with the premolar position (P = .0594), sex of the patient (P = .650), pulpal inflammatory reaction (P = .613) or the time elapsed since surgery (P = .531). Restoration with zinc oxide eugenol was found to negatively influence tertiary dentin matrix secretion (post hoc analysis of variance, P = .030).

Conclusions. The age of a patient at treatment, the choice of restorative material and the size of the restoration preparation are all factors that can positively or negatively affect the pulpal repair response.

Clinical Implications. Age of the patient affects dentin repair capacity and may be a factor in treatment planning decisions. Minimizing the cutting of dentin, especially the width and base of the preparation, reduces the probability of recurrent pulpal complications.

The tooth pulp detects and responds to dentin injury resulting from caries, attrition, abrasion, erosion, trauma and restorative dental procedures. The deposition of a tertiary dentin matrix is the main pulpal repair response to these injurious conditions.1–5 Unlike primary or secondary dentin, which forms along the entire pulp-dentin border, tertiary dentin is secreted focally by odontoblasts in response to primary and secondary dentin injury. The process of tertiary dentin secretion can be classified as being reactionary or reparative in origin, depending on the severity of the initiating response and the conditions under which the newly deposited dentin matrix was formed. In general, reactionary dentin is secreted by pre-existing odontoblasts and reparative dentin is secreted by newly differentiated odontoblastlike cells.6 The secretion of reactionary dentin is the main postoperative odontoblast repair response to a restoration preparation being carefully cut into the dentin of a tooth.

The difficulty with measuring pulpal responses to a preparation cut into dentin is that the pulpal reactions are the end result of all the preparation and restoration events. All the events involved must be factored into the pulpal response; for example, method of preparation,7 condition of the dentin restoration wall,8 presence of bacteria,9 the application method of restoration material10,11 and pulpal inflammation.12 The relative importance of these multiple events varies somewhat from one restoration to another and from one patient to another. The successful outcome of restorative treatments, however, depends in part on understanding and making treatment decisions that are congruent with the natural repair responses of the tooth. No artificial material exists that can be placed into a tooth that provides better protection for the pulp than dentin.13 Evidence is accumulating to show that the effects of a restorative preparation, especially the residual dentin thickness, or RDT, may play a greater role in the stimulation of reactionary dentin than irritation to or toxicity of the restorative material.14–18 The exact nature of this relationship, however, is unclear.

The aim of this work was to establish the quantitative relationship between tooth injury in the form of restoration preparation and the tooth’s natural repair response by reactionary dentin secretion.


   SUBJECTS, MATERIALS AND METHODS
TOP
 ABSTRACT
 SUBJECTS, MATERIALS AND METHODS
RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Twenty-seven patients—13 male and 14 female—between 9 and 17 years of age, had Class V restorations prepared in noncarious intact first or second maxillary premolars (13) or mandibular premolars (14) that had been scheduled for orthodontic extraction at the Dental Hospital of Marseille, Marseille, France. After a postoperative interval of 28 to 163 days and receipt of the patients’ or their parents’ or guardians’ informed consent, we administered local anesthetic and extracted the teeth. Then we polished the teeth with pumice paste to remove plaque and calculus, before the operative procedure. The tooth surface was isolated with sterile cotton rolls, and saliva was controlled with high-speed evacuation. We placed the Class V preparations in the buccal surface, 1 millimeter above the level of the cementoenamel junction and made preparations by intermittently applying the rotary hand-piece with water spray to remove the enamel. Preparation forms were then cut into the tooth dentin with a bur using the least possible pressure at a drill speed of 4,000 revolutions per minute with water spray coolant. Preparation forms were cut into the dentin to a range of residual dentinal thicknesses and axial floor widths to a maximum of 2.27 mm. The floors of the preparations were kept curved and parallel to the outer surface of the tooth. The walls of the preparations immediately were conditioned with a 17 percent dis-odium ethylene diamine tetra-acetate solution, pH 8 for 15 seconds, flushed with sterile water for five seconds and dried with a light airstream for two seconds. Teeth were randomly assigned to three experimental groups for restoration.

We used an amalgam (Contour, Kerr) to restore 17 preparations, in conjunction with a calcium hydroxide lining material (Dycal, Dentsply). Seven additional preparations were restored with zinc oxide eugenol, or ZOE, (Kalzinol, Dentsply); an additional three restorations were restored with a reinforced ZOE product (Intermediate Restoration Material, De Trey Dentsply). All materials were prepared and used according to the manufacturers’ instructions.

At the end of the postoperative period, the extracted teeth were fixed in 10 percent neutral-buffered formalin for 24 hours, demineralized in a sodium formic acid solution (3.4 percent sodium formate in 15 percent formic acid) for 21 days, and then routinely processed and embedded in paraffin wax for histologic examination. We cut sections at 6 micrometers and routinely stained them with hematoxylin and eosin.

We categorized the pulpal inflammatory responses as either slight, moderate or severe on the basis of previously published criteria19

– A severe response indicated the complete disintegration of the odontoblasts, microabscess formation related to the preparation floor and pulpitis-type edema in the pulp core.
– A moderate response was characterized by localized hyperemia or hemorrhages containing scattered leukocytes of the acute or chronic series, depending on the postoperative interval, as well as a reduction of the uniform odontoblast cell layer into an irregular layer with signs of incipient inflammation.
– A slight inflammatory response manifested as the presence of hemorrhages and circulatory stasis in the sub-odontoblastic region at the base of the preparation floor but with an underlying normal, multilayer, odontoblast cell distribution.

The area of reactionary dentin was estimated histomorphometrically at x10 magnification, using a grid eyepiece graticule. The RDT between the base of the prepared tooth and the odontoblastic surface also was measured using the grid eyepiece graticule.20

We examined the raw numerical data from all the experiments using linear regression analysis of variance, or LRA-NOVA, tests (StatView software, SAS Inc.). We also used analysis of variance, or ANOVA, tests (SuperANOVA software, SAS Inc.) to compare the difference between means when the data were categorical. ANOVA post hoc tests 21 were used to compare the differences between categorical variables. These procedures are reportedly among the most versatile and most conservative of the multiple comparison tests.22


   RESULTS
TOP
 ABSTRACT
 SUBJECTS, MATERIALS AND METHODS
 RESULTS
DISCUSSION
 CONCLUSION
 REFERENCES
 
Identification of reactionary dentin. A histomorphological evaluation of the extracted pre-molar specimens revealed the presence of a tertiary dentin matrix, showing tubular continuity between the secondary dentin matrix and the pre-existing odontoblasts. These observations are necessary to classify the secreted dentin matrix as being reactionary in origin.23

Residual dentin thickness. The cutting of tooth dentin for restoration preparation proved to be a powerful stimulus for the initiation and progression of a reactionary dentinogenic response (Table 1Go). Reactionary dentin was found to be deposited at the odontoblast–secondary dentin interface beneath areas where the dentin tubules had been cut. For every 1-mm decrease in the RDT between the floor of the preparation and the odontoblastic surface (Figure 1Go), the mean area of reactionary dentin matrix increased by 1.187 square millimeters (Table 2Go).


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  		TABLE 1 REACTIONARY DENTIN AREA (SQUARE MILLIMETERS) VS. VARIABLES.

 


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  		Figure 1. Regression plot of the reactionary dentin area secreted vs. the residual dentin thickness of prepared restorations.

 

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  		TABLE 2 REACTIONARY DENTIN AREA (SQUARE MILLIMETERS) VS. CORRELATED VARIABLES.

 
Patient age. The area of reactionary dentin deposit was found to be partially dependent on the patient’s age (Table 1Go). The area of reactionary dentin deposited after a tooth was repaired had a tendency to increase as the age of the patient increased (Figure 2Go). The mean increase in the area of the reactionary dentin deposit was 0.163 mm2 for every year of age (Table 2Go).



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  		Figure 2. Regression plot of the reactionary dentin area secreted vs. the patients’ ages.

 
Preparation floor surface area. The area of reactionary dentin secreted after a tooth was prepared appeared to increase as the axial floor surface area of the preparation cavities was increased (Table 1Go). There did not, however, appear to be a clear relationship between the total preparation surface area (axial floor and occlusal/cervical walls) and the subsequent secretion of reactionary dentin (Table 1Go). The mean reactionary dentin area was increased by 0.407 mm 2 for every 1-mm2 increase in the preparation floor surface area (Table 2Go).

Preparation width. The mean area of the reactionary dentin deposits appeared to increase in response to an increase in the diameter width of the preparations (Table 1Go). The mean reactionary dentin area increased by 1.064 mm2 for every 1-mm increase in the width of the preparation (Table 2Go).

Restoration material. The combined ANOVA statistic for the effects of restorative materials was P = .0530 (Table 1Go). Amalgam, Intermediate Restorative Material, or IRM, and ZOE test products were evaluated, and the choice of restoration product appeared to influence the tooth’s reactionary dentinogenic activity (Figure 3Go). Restoration with ZOE appeared to have a negative effect on the dentinogenic process compared with amalgam (post hoc ANOVA, P = .0301). The difference in reactionary dentinogenic activity after restoration with IRM and with amalgam products was not found to be statistically significant (post hoc ANOVA, P = .544).



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  		Figure 3. Bar chart of the mean reactionary dentin area secreted beneath restorative materials.

 
Variables with an insignificant correlation to the reactionary dentin response. The following variables were found to have an insignificant correlation with the area of the reactionary dentin deposits: mandibular or maxillary premolars, preparation and restoration size, sex of the patient and premolar dentin thickness (Table 1Go). The size of the reactionary dentin deposits did not increase over time as the postoperative period between tooth cavity preparation and extraction was increased from 28 to 163 days (Figure 4Go) (Table 1Go). An insignificant correlation also was found between postoperative inflammatory activity and reactionary dentin secretion (Table 1Go), as well as the RDT and the postoperative inflammatory activity (LRANOVA, P = .464).



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  		Figure 4. Regression plot of the reactionary dentin area secreted vs. the postoperative period.

 
Control: analysis of the residual dentin thickness within groups to ensure that the test comparisons were valid. To remove the possible influence of a mismatch of RDTs between each of the restoration variables, the RDTs were measured and compared with each other using ANOVA statistics. No statistical differences were observed at the P = .05 significance level for age of the patient (P = .661), preparation floor surface area (P = 0.297), preparation width (P = .343), restorative material (P = .519) or any of the other preparation variables. Therefore, the effect of the RDT could be excluded from being the cause of a significant change in the area of reactionary dentin between any of the restoration variables described in Tables 1Go and 2Go. The R2 correlation coefficient of the LRANOVA restoration variables were found to be within the range of R2 = .369 to 0.251. R2 correlation coefficients higher than R2 >.25 reportedly show a fair degree of relationship between variables.22


   DISCUSSION
TOP
 ABSTRACT
 SUBJECTS, MATERIALS AND METHODS
 RESULTS
 DISCUSSION
CONCLUSION
 REFERENCES
 
The methods used in this study to examine the pulpal postoperative repair responses attempted to separate the effects of preparation, restoration and patient factor variables. The quantity of the reactionary dentin secreted in permanent premolar teeth appeared to increase as the age of the patient was increased, irrespective of a restoration’s residual dentin thickness. For example, a mean area of reactionary dentin secreted after a premolar was prepared in a 10-year-old is estimated to be only 21 percent of that secreted in a 17-year-old, as the mean area of reactionary dentin increases by 0.163 mm2 for every year of age (Table 2Go).

The change in dentinogenic activity of the restored teeth of patients with different ages can be attributed to maturation-related changes within the dental pulp.24–26 Although the regression graph (Figure 2Go) showed that the area of the reactionary dentin increased progressively with age, this could not be expected to be representative of the tertiary dentinogenic activity of a tooth into old age. The premolars studied in this sample were newly erupted in the younger patients and were still developing to a mature state in the older patients, thus the reactionary dentinogenic response appeared to intensify with tooth maturation.

Age has been observed to have a role in the deposition of reactionary dentin.27 The dentinogenic response potential of teeth could be expected to reach a maturation plateau and thereafter diminish into old age. A reduction in the speed of secondary dentinogenesis has been observed in the elderly,28 and the repair of dentin is thought to be mediated by analogous molecular and cellular interactions.29 Animal models also have shown that the quality of the tertiary dentinal response diminishes with age.30

Our understanding of the changes in pulp and dentin due to maturation, aging and disease processes is still in its infancy, but the increased danger when treating young and elderly patients is that the dentinal repair response will be inadequate to provide pulp protection, and pulp complications will recur. The impact of these observations on future treatments is expected to be profound.31 The quantity of reactionary dentin secreted in response to the tooth preparation appeared to be almost identical in female and male patients (ANOVA, P = .650). This was despite the fact that premolar eruption can be observed more than one year earlier in females than in males.32 Similarly, there did not appear to be any statistically significant differences between variables in maxillary and mandibular premolar teeth.

This study demonstrated a quantitative relationship between the RDT and the stimulation of reactionary dentinogenesis. Surprisingly, the size of a restoration was not found not to be closely correlated to the reactionary dentinogenic activity (LRANOVA, P = .308). The mean area of reactionary dentin in a restoration with an RDT of 1.5 mm was estimated to be 10.6 percent of the amount formed beneath a restoration with an RDT of 0.5 mm (Table 2Go). The exact reason for the inverse relationship between the restoration’s RDT and the formation of reactionary dentin matrix is not clear, but it does give an insight into the mechanism of dentin injury transduction to the odontoblast cells. The odontoblast process has a clearly defined role in the transport of secretory vesicles and their release into the extracellular space.33 The role of the process in communicating dentin damage to the odonto-blast cells is much less certain. Some studies have suggested that the processes extend through only one-third of the dentinal tubules’ length.34,35 In reality, the length of the odontoblast process is probably variable, and so the operation of this dentinal injury transduction system in isolation would not adequately explain the ability of the odontoblasts to respond to peripheral dentin injury.36 Despite the considerable controversy regarding the odontoblastic process and even the contents of the tubule lumen,37 the role of these structures in forming some part of the dentinal injury transduction system cannot be discounted.

Alternatively, the relationship between the odontogenic response and an increased RDT may support the theory that a molecular stimulus for reactionary dentinogenesis is an effecter molecule—perhaps a growth factor—that has been solubilized from the reservoir of endogeneous growth factors contained within the dentin matrix.38,39 The RDT of a preparation is directly proportional to the dentinal tubule length and inversely proportional to the dentin permeability,40 so a reduction in the RDT would increase the concentration of the effecter molecule(s) acting at the level of the odontoblast cell body. When recombinant human osteogenic protein-1 is applied to freshly cut dentin it has been found to stimulate significantly more reparative dentin than calcium hydroxide paste in monkey teeth.41,42 Transforming growth factor-ß, or TGF-ß, and related members of this family are known to influence bone matrix synthesis and have been shown to modulate the synthesis of collagens and proteoglycans.43 Recently, TGFß1- and -ß3 isoforms have been demonstrated to stimulate odontoblast dentinogenic activity at local sites of application.44 These findings one day may provide clinicians with additional options for the treatment of substantially damaged or diseased teeth,45 especially in young and elderly patients.

A correlation was discovered between the secretion of reactionary dentin matrix and the size of the floor surface area of the preparations (LRANOVA, P = .0266), but not the whole surface area of the preparations (LRANOVA, P = .435). The mean area of reactionary dentin secreted after a restoration preparation with a floor surface area of 1.5 mm2 was calculated to be 18.83 percent of the quantity secreted beneath a restoration with a base surface area of 4 mm2. In a similar fashion to the base surface area, the width of the restoration preparations also was found to correlate well with the quantity of reactionary dentin secreted (ANOVA, P = .0415). As the width of the cavity preparations was increased from 1.4 to 2.2 mm, the mean area of reactionary dentin secreted increased by 437.2 percent. The oversecretion of reactionary dentin potentially could cause "pulpal strangulation" and hence death. Thus, tooth preparations should be performed only when needed and using the least traumatic method possible to minimize the magnitude of the reactionary secretory response.

The correlations discovered between the quantity of reactionary dentin secreted by the odontoblasts and the preparation’s floor surface area and width—but not the whole preparation surface area—might suggest that the main pathway for dentin injury transduction involves intertubular dentin structures. Feedback to the odontoblasts via the inter-tubular dentin system, rather than via the intratubular dentin matrix infrastructure, would tend to support the hypothesis that growth factor(s) could diffuse down the dentinal tubules46 and interact with the odontoblasts to stimulate the secretion of reactionary dentin matrix.

The detection of dentin damage, its transduction to the odontoblasts, the stimulation of the odontoblast secretory activity and the secretion of a reactionary dentin matrix appeared to be accomplished within 28 days of surgery (Figure 4Go). This would be in agreement with the findings of Bjørndal and colleagues47 that reactionary dentin secretion was observed only in response to active lesions. The fast secretion of this reactionary dentin matrix appeared to confirm its purpose as a dentin of repair. Reparative dentinogenesis, on the other hand, which requires the replacement of damaged odontoblasts and the differentiation of a new generation of odontoblastlike cells, has been reported to have a lag time, before its tertiary dentin secretory activity is fully activated and completed.48,49

The oversecretion of reactionary dentin potentially could cause ’pulpal strangulation’ and hence death.

Although reparative and reactionary dentinogenesis are two distinct processes, it is possible to have both reparative and reactionary dentins superimposed on one another.50 The basis for a biological approach to clinical practice would be to use the reaction potentials of the tissues intentionally. Several reaction patterns of dentin have been demonstrated that may be put into clinical use directly.51 This study, however, has demonstrated that there is no sound medical basis for altering operative dental treatments for a particular sex or for a maxillary or mandibular premolar position. All have a similar dentin repair capacity.

Whenever the pulp is affected by caries or by mechanical, chemical or physical trauma, the immune system will trigger an inflammatory response to limit tissue damage by eliminating and digesting invading organisms and cell debris. Paradoxically, these inflammatory reactions can injure the pulpal cell populations, and in the most severe cases, obliterate the whole tooth pulp. In this study, different categories of inflammatory activity caused by tooth preparation and restoration had only a slight effect on the secretion of reactionary dentin (ANOVA, P = .6133). The relatively rapid speed of the reactionary dentinogenic process may minimize the possible deleterious effect of the pulpal inflammatory response. The RDT may have been expected to be one of the factors, which could affect the postoperative severity of the pulpal inflammatory activity,52 but no evidence was found to support this hypothesis (LRANOVA, P = .464). This finding is probably indicative of the complex situation regarding the stimulation of the pulpal inflammatory activity, which can involve such factors as microleakage.53

In general, it can be concluded that an inflammatory response severe enough to injure the odontoblasts and the other pulpal cell populations also will damage the tertiary dentinogenic activity of the tooth. More studies are needed to better understand the process of dentinogenesis and the role played by the odontoblast.54,55 When this knowledge becomes available, however, it may permit improved treatment modalities for the injured pulp to be devised.56 A better understanding of the factors that can negatively or positively control the dentinogenic process could increase the clinical success of many restorative tooth treatments and avoid pulpal strangulation and death.57

The restoration of preparations with calcium hydroxide as a liner beneath an amalgam filling or with an IRM did not appear to influence the inherent dentinogenic activity of the tooth (ANOVA, P = .544). The use of ZOE as a restorative material, however, appeared to cause a significant reduction in the secretion of reactionary dentin matrix (ANOVA, P = .0301). This finding has been observed in other studies.58,59 The high cytotoxic activity of ZOE could interfere with cellular respiration60 and negatively influence reactionary dentin secretion by the odontoblast cells since the supply of oxygen is necessary for dentinogenic activity.61 In certain clinical situations, such as in the restoration of wide preparations, ZOE or similarly acting materials could be used as a lining agent to minimize the risk of pulp strangulation by reducing reactionary dentin secretion.


   CONCLUSION
TOP
 ABSTRACT
 SUBJECTS, MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
REFERENCES
 
Postoperative pulpal responses and reactionary dentin repair have been characterized. The influence of the patient’s age on dentin repair response has implications for the treatment planning of many dental conditions. In terms of reactionary dentinogenesis, although the restorative material can be influential, its effect is subservient to the direct relationship between the quantity—number and length of time—of operative dental preparation procedures and the magnitude of the reactionary dentin repair response. Using an appropriate, high-quality restorative material is important, but its use cannot supersede the expertise and surgical skill of the clinician in shaping and minimizing the removal of iatrogenic teeth when creating preparations in such a way as to reduce the probability of recurrent pulp complications.


   FOOTNOTES
 

Mr. Murray is a postgraduate student, School of Dentistry, The University of Birmingham, England.


Dr. About is a lecturer, Faculte d’Odontologie, Interface Matrice Extracellulaire Biomateriaux, Marseille, France.


Dr. Lumley is a senior lecturer, Restorative Dentistry, School of Dentistry, The University of Birmingham, England.


Ms. Smith is a researcher, School of Dentistry, The University of Birmingham, England.


Dr. Franquin is a senior lecturer, Faculte d’Odontologie, Interface Matrice Extracellulaire Biomateriaux, Marseille, France.


Dr. Smith is professor of oral biology, School of Dentistry, Faculty of Medicine and Dentistry, The University of Birmingham, St. Chad’s Queensway, Birmingham, England, B4 6NN. Address reprint requests to Dr. Smith.


The authors thank Mirelle Remusat, B.Sc., of the Université de la Mediteranee, Marseille, France, for her technical skills, as well as Thomas W. Smyth, B.Sc., of the University of Minnesota, Minneapolis, and Yousef Al-Dlaigan B.D.S., M.Sc., of the University of Birmingham, England, for their advice.


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 ABSTRACT
 SUBJECTS, MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 

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