Discussion - References.
Radiographic plates and endocator equipment can be used to provide estimates of cavity RDT, but these measurements do not reflect the physiology of dentine. Measurement of dentine tubules along their length appears to represent the most logical and physiologically relevant method (Langeland & Langeland 1966). In this study, RDT was measured as the shortest distance from the cavity floor to the pulp tissue, primarily because of ease of use and avoidance of measuring complications between different points. The advantage of measuring RDT using this method is that it can be used in conjunction with conventional clinical techniques. Although a relationship probably exists between RDT and tubule length, especially in deep cavities, there is a clear need to evaluate pulp responses in conjunction with dentinal tubule length in future studies. Nevertheless, this study has shown how the CWD can be used to estimate RDT because of the uniformity of premolar dentine thickness together with careful cavity positioning. In lingual, occlusal and buccal cavities, the maximum dentine depth of cavity preparation before pulp exposure takes place was found to be 2.33, 1.96 and1.1mm, respectively. Whatever approach is used to estimate the RDT of cavity preparations prior to their restoration, it is clear that the interactions between RDT, cavity preparation and restoration variables are important to the understanding of the injuries sustained to the dental pulp, and its capacity to mediate dentine repair and remain vital throughout life. The basis for a biological approach to clinical practice would be to identify and attempt to reduce sources of tissue injury, such as using the pulp-protective effect of dentine beneath the cavity floor as well as incorporating the dentine repair capacity of teeth as part of treatment. Several reaction patterns of dentine repair have been demonstrated that may be put into clinical use directly (Mjor 1985, 2002). This requires an understanding of the pulpal responses to varying cavity RDTs and to the reactivity and reaction patterns of primary dentine. Studies of human teeth have shown a high prevalence of histological responses to cavity preparation and restoration events. Dentine bridge formation has been observed in 90% of teeth following pulp exposure (Baume 1980) and reactionary dentine secretion has been observed beneath more than 50% of restorations (Murray et al.2000a,b). Severe categories of pulp inflammation have been associated with low RDTs (Hebling et al.1999). In this present study, only three of10 exposed pulps were associated with dentine bridge secretion and only seven of 88 (8%) non-pulp-exposed cavity preparations were associated with reactionary dentine secretion. A possible explanation for this variation may be due to differences in the observation periods. The mean observation time was approximately 27 days in this study versus 46 and 64 days in other studies similarly evaluated (Murray et al.2000a,b).The shorter time frame of this present study would have provided less time for the dentine repair processes to be fully accomplished. Other explanations for these differences include a variation between patient samples, including the possible effects of treatment history and other factors such as age. The prevalence and magnitude of pulpal responses could theoretically be dependent on subjective criteria that are difficult to measure quantitatively, such as variations in the healing response between individual patients and differences in clinical technique between clinicians. Little is known about the importance of these factors and it was not possible to address the mint his present study. Consequently, we have focused on pulp-dentine responses to RDT or pulp exposure, which is somewhat under the control of the clinician.
In an attempt to overcome difficulties with the use of subjective qualitative criteria, quantitative approaches were used, whenever possible, to assess pulp activity under controlled conditions of patient age, health and specimen tissue preparation. This is because qualitative data always contains an element of subjectivity (Warfvinge1987). The application of the anova multiple comparison test avoided the problem of having to compute many individual comparison tests between histological raw data (Qvist & Stotlze1982). If this test were not performed, the multiple tests between different pairs of means would alter the a-level, not for each comparison, but for the experiment as a whole. For example, if the six pairs of means shown in Fig. 4 are compared using individual tests, and if each comparison is made by using a ј 0.05, there is a 5%chance that each comparison will falsely be called significant, i.e. a type I error would occur six different times. Overall, therefore, there is a 30% chance (6 _5%) of declaring one of the comparisons incorrectly significant. The use of nova by the authors overcame these problems and in agreement with Dawson- Saunders & Trapp (1994) provided a versatile and conservative statistical method.
Many factors have been suggested to injure the pulp, including cavity preparation trauma, restorative dental procedures, operator hand instrumentation, systemic diseases, caries, attrition, erosion, chemicals, dental materials 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 factors correlated with pulp injury have proved to be controversial. Clearly, the RDT or proximity of the injury stimulus to the pulp tissue will have some impact on the severity of pulp response. Often a reduction in proximity of the cavity floor to the pulp tissue has been reported to increase reactionary dentine deposition (Murray et al. 2000b), whilst other studies have reported little correlation between RDT and reactionary dentine activity (Stanley 1961, Santini & Ivanovic 1996). The present study did not demonstrate a relationship between the RDT and the presence of reactionary dentine. This lack of correlation may be related to the minimal nature of the responses observed, resulting from the short postoperative extraction schedule. However, the formation of a dentine bridge was correlated to the creation of a pulp exposure. This would suggest an accord with previous investigations that cavities prepared close to the pulp tissue can injure the underlying odontoblast cells (Darvell1981, Lee et al.1992). Injury to the odontoblasts may explain the loss of capacity of these cells to secrete reactionary dentine, and the secretion of dentine bridge by a new generation of odontoblast-like cells (Smith et al.1994).
The effect of restorative materials on pulpal activity has similarly proved to be controversial. Some types of restorative materials, such as Ca(OH)2-based products have been reported to stimulate pulpal repair activity by increasing reactionary dentine deposition (Stanley 1968), whereas some other studies have shown the effects of the restorative material on pulp responses are minimal (Cox 1992). This present study did not demonstrate a relationship between reactionary dentine secretion and the pure form of Ca(OH)2 mixed with water as a material liner. This may be due to the precipitation of crystalline salts within the dentinal tubules, reducing their permeability and preventing any adverse reactions in the pulp (Mjor & Ferrari 2002).The results from this study were also in agreement with previous observations, indicating the negative effect of ZOE (Stanley 1968, Kirk & Meyer 1992) and amalgam on reactionary dentine secretion. A smaller RDT was required to observe reactionary dentine with ZOE and no reactionary dentine was associated with amalgam, although amalgam was only used to restore very shallow cavity preparations. Therefore, the larger RDT may be responsible for the lack of reactionary dentine, rather than the chemical activity of amalgam, because reactionary dentine activity is reduced with increasing RDT (Stanley et al. 1966). The therapeutic significance of why some restorative materials may be associated with larger areas of reactionary dentine is difficult to explain because of the limited information available.
However, changes in the buffering effect of dentine with different RDTs can influence the cytotoxicity and chemical activity of restorative materials on underlying pulp tissue (Murray et al. 2000c). Alterations in dentine physiology and chemistry in differing tooth locations may also be able to explain some differences. For example, Ca(OH)2 on primary dentine will quickly cause precipitation of mineral salts within the tubules (Mjor et al. 1961, Mjor & Furseth1968) and that will reduce dentine permeability and influence pulp tissue reactions. This biologically positive effect can be used to prevent reactions from restorative materials when Ca(OH)2 is used as a liner (Mjor1963).
Some areas of coronal dentine show marked variation in the structure of the tubules, e.g. the tubules in the most pulpal dentine in newly erupted teeth have no discernible peritubular dentine lining them whilst those in the bulk of dentine are relatively uniform and are lined by peritubular dentine (Mjor 1966). The structure and reaction potentials of this dentine will vary depending on the age of the patient and wear/attrition amongst other factors that may have affected the tissue. In teeth from young individuals, the dentine will be truly unaffected and therefore more permeable than the dentine in the central part of the cavity preparation, which may have mineralized due to caries. This situation calls for particular attention to the protection of the most peripheral part of cavity preparations, and of large parts of crown preparations, especially those on intact teeth of young individuals (BjMrndal & Mjor 2001).
Cavity positioning is also important because the area of tubules exposed by the preparation can vary from about 80%of the total area in deep preparations in teeth from young individuals to 4% in preparations in the peripheral part of the dentine in teeth from individuals in any age group (Ketterl1961). Consequently, the buffering effect of dentine tubule structure in preventing the progression of caries, leakage of bacteria and penetration of chemicals, appears to be just as important as the RDT in providing pulp protection (Mjor & Ferrari 2002).
The combined effects of bacteria and their toxins has been strongly associated with increased pulpal inflammatory activity. This inflammatory activity has been associated with injury to pulpal tissue and reductions in the numbers of vital cell populations (Brannstrom 1984, About et al. 2001b). The absence of bacteria at the cavity margins in this present study probably explains the lack of pulpal inflammatory reactions and the failure to identify any significant correlation between cavity RDT and pulpal inflammation. This suggests that pulpal inflammation is not primarily stimulated by the effects of cavity preparation followed by restoration with Ca(OH)2, amalgam or ZOE. However, the RDT of preparations may be critical in modifying pulpal responses to more injurious restorative materials, such as adhesives (Hebling et al. 1999) and also in the presence of caries and bacteria.
This study has provided evidence to highlight the complex interplay between restorative materials, cavity RDT and cavity dimensions which can interact together to injure the pulp tissue. Clearly, cavity RDT plays a central role in determining the extent of pulpal injury and repair responses. The mechanisms involved in the detection of dentine damage, its transduction to the odontoblasts and the stimulation of increased odontoblast dentine synthesis and secretion remain incompletely understood (Kardos et al. 1998). However, damage to the odontoblastic process, injury to the intratubular elements, nerve damage and the presence of bioactive molecules solubilized from the injured dentine matrix, may be involved (Smithet al.2001).Currently, following cavity restoration, a high proportion of teeth with vital pulps exhibit symptoms requiring endodontic treatment (Zollner & Gaengler 2000). Although the mechanisms of odontoblast peritubular and tertiary dentine secretion remain incompletely understood, the ability to anticipate and manipulate its activity should form part of treatment planning. The basis for a biological approach to clinical practice would be to identify and attempt to reduce sources of tissue injury, and also exploit the dentine repair capacity of teeth intentionally as part of treatment. This should help to minimize postoperative complications following restorative treatment. An improved understanding of the degree of pulp responses to varying RDTs will help with the identification of pulpal complications.
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