Discussion.
A dentinal bridge may be a sign of healing or irritation (Schuurs et al. 2000) and it is known that the presence of bacteria is a significant factor in inhibiting healing of pulp exposures (Watts 1979, Browne et al. 1983, Cox 1987).Unfortunately, calciumhydroxide does not adhere to dentine and lacks the ability to seal. Tunnel defects in dentine bridges under calcium hydroxide dressings can act as pathways for microleakage (Cox et al. 1985). This material also has a tendency to dissolve over time (Schuurs et al. 2000).
Although a statistical analysis was not performed in this study, due to the small number of samples, the results show that inflammation was seen more frequently and with a greater severity in samples capped with calcium hydroxide. With MTA , thicker bridges formed and the presence of an odontoblastic layer was a frequent finding. In addition, few samples capped with MTA had hyperaemia, whereas hyperaemia was seen in every sample capped with calcium hydroxide, and virtually no odontoblastic layer was formed. Necrosis was also a more frequent finding with calciumhydroxide. It should be emphasized, however, that these results are relevant for only small exposures created mechanically and without caries.
Cox et al. (1985) and Cox (1987) used ZOE to prevent bacterial leakage as in the present study, so that inferior results with calcium hydroxide compared to MTA cannot be attributed to leakage. Staining bacteria in histological sections is difficult and may not show bacteria despite their presence in the samples (Mjor1977). In this study, no sections were stained for bacterial invasion of the site.
Abedi et al. (1996) found a significantly higher frequency of calcific bridge formation and less inflammation with MTA compared with calcium hydroxide in an animal study. Pitt Ford et al. (1996) also showed dentine bridge formation in all pulps capped with MTA and no inflammation except in one sample. In contrast, all samples capped with calciumhydroxide preparation showed pulpal inflammation, and bridge formation occurred in only two samples. In accordance with these and the present study, Junn et al. (1998) reported significant differences between the amount of inflammation and the degree of dentinal bridge formation in the MTA and calciumhydroxide groups of 63 teeth from four Beagle dogs.
The ability of MTA to induce the formation of a dentine bridge may be due to its excellent sealing ability (Torabinejad et al. 1993, 1994, Bates et al. 1996, Fischer et al. 1998, Wu et al.1998) or biocompatibility (Kettering & Torabinejad1995, Torabinejad et al.1997, 1998, Holland et al. 1999, Mitchell et al. 1999, Keiser et al. 2000). MTA can induce cytokine release from bone cells (Koh et al.1995, 1997, 1998) and can allow the attachment of osteoblasts in the form of a monolayer (Zhu et al. 2000); however, some studies suggest that it is only osteoconductive and not osteoinductive (Moretton et al.2000). It has sufficient compressive strength to allow condensing of amalgam and a negligible solubility (Torabinejad et al. 1995).
However, Myers et al. (1996) found no significant differences in pulpal status or bridging between MTA and calcium hydroxide groups of their study on dogs. They concluded both MTA and calcium hydroxide performed equally well as pulp-capping agents. It has not been possible to identify whether the inductive effects of calcium hydroxide are due to release of calcium or hydroxyl ions (Schubich et al.1978) and early work has suggested calciumions are not necessary for the repair process (Glass & Zander1949, Seltzer&Bender1958). Despite many studies, the mechanism of action of this material remains unknown (Pashley1996).
Faraco & Holland (2001) emphasized the advantages of MTA over calcium hydroxide for pulp capping. Thirty teeth of three dogs were capped with either calcium hydroxide or MTA. More inflammation and less frequent dentinal bridging were observed in the calcium hydroxide group in addition to material resorption and microleakage of microorganisms. However, a subjective method of evaluating inflammation had been employed.

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