Introduction.
P. E. Murray, A. J. Smith, L. J. Windsor & I. A. MjorOral Biology, Indiana University School of Dentistry, Indianapolis, IN, USA.
Oral Biology, School of Dentistry, The University of Birmingham, Birmingham, UK.
NIOM, Scandinavian Institute of Dental Materials, Oslo, Norway.
College of Dentistry, University of Florida, Gainesville, FL, USA.The importance of the remaining dentine thickness (RDT) underlying cavity preparations in modifying pulp responses to dental materials has been a topic of controversy for more than a century (Stanley et al. 1975). Over the years, the estimated value of the minimal cavity RDT which does not cause pulp injury has been decreasing. Stanley (1994) suggested that a RDT of 2 mm would protect the pulp from injury caused by most restorative materials and procedures. Subsequently, Pameijer et al. (1991) reported during luting procedures that a RDT of 1mmor more would be sufficient to protect the pulp tissue from the cytotoxic effects of zinc phosphate (ZnP) and resin-modified glass ionomer (RMGI). Nevertheless, it was recently suggested that restoring deeper cavity preparations, carefully cut down to 0.5 mm, with zinc oxide eugenol (ZOE), intermediate restorative material (IRM) and calcium hydroxide (Ca(OH)2)/amalgam, appeared to have little effect on underlying odontoblast numbers for up to 381 days following treatment in patients (Murray et al. 2000b). Moreover, it is unclear if the minimum RDT, at which little or no pulp injury can be observed, varies significantly between different patient variables and restorative materials. An important source of pulp injury is likely to be the increased traumatic operative procedures involved in cutting deeper cavity preparations (Stanley 1961, Darvell 1981). Understanding the interactions between RDT and the degree of pulp injury may be important in understanding why some vital teeth exhibit clinical symptoms leading to the need for endodontic treatment (Zollner & Gaengler 2000). Nevertheless, precise information on the role of the cavity RDT in influencing pulpal injury and dentinal repair responses with common restorative materials is limited (Lee et al. 1992, Murray et al. 2001).
The buffering effect of the cavity RDT to provide pulp protection can be expected to vary not only with dentinal tubule distance from the prepared cavity floor to pulp tissue, but also with dentinal tubule permeability. Tubule permeability is an important factor in allowing the progression of caries, bacterial leakage and chemical irritants towards pulp tissue (Mjor & Ferrari 2002). Consequently, the width of affected tubules and the peritubular secretion of dentine in reducing their width to help mediate pulp protection are important. Peritubular secretion takes place throughout life and is most noticeable in the teeth of older patients, and in those that have experienced wear/erosion (Mjor 2002).
In newly erupted teeth, the most pulpal dentine often has no discernible peritubular dentine lining (Mjor 1966).Therefore, the permeability and peritubular reaction potentials of teeth may be expected to vary with patient age and treatment history, suggesting that although the RDT between patients can be similar, dentine permeability and pulp reactions may be quite different (Mjor et al. 2001). Nevertheless, it is important to characterize human pulp responses to RDT following treatment to gain an improved understanding of pulp- dentine responses to cavity preparation and restoration variables.
Evidence suggests that reductions in the RDT of cavity preparations, increasingly make the pulp susceptible to traumatic injuries caused by cavity preparation and restoration events (Santini & Ivanovic 1996, Murray et al. 2000a).Thus, it is important to avoid needless dentine removal during surgery. Nevertheless, often the RDT of cavity preparations will be determined by the extent of disease progression and treatment regime. Accordingly, it is important to quantify the degree of pulp injury in response to a range of cavity RDTs in combination with common restorative materials, such as Ca(OH)2/amalgamand ZOE. Few studies have attempted to quantify pulp injury as a function of RDT, restoration materials, or other cavity restoration variables, such as cavity width and cavity wall depth. Nevertheless, minimizing pulp injury following treatment and preserving the numbers of pulpal cell populations, particularly the odontoblasts, can be critical to maintain function and vitality of the pulp, as well as reducing the probability of postoperative complications (About et al. 2001a).
The aims of this study were to quantify pulp responses to cavity RDT by measuring and correlating patient variables such as age, cavity preparation variables such as tooth type, tooth surface of cavity preparation, tooth dentine thickness, cavity floor width and cavity wall depth, as well as restoration variables, including the time elapsed since restoration and type of restoration material. Pulpal responses were measured using odontoblast and subodontoblast cell numbers, pulpal inflammation, as well as dentine bridge and reactionary dentine formation.