The importance of inflammation has been underestimated in pulpal healing, and in the past, it has been considered only as an undesirable effect. Associated with moderate inflammation, necrosis includes pyroptosis, apoptosis, and nemosis. There are now evidences that inflammation is a prerequisite for pulp healing, with series of events ahead of regeneration. Immunocompetent cells are recruited in the apical part. They slide along the root and migrate toward the crown. Due to the high alkalinity of the capping agent, pulp cells display mild inflammation, proliferate, and increase in number and size and initiate mineralization. Pulp fibroblasts become odontoblast-like cells producing type I collagen, alkaline phosphatase, and SPARC/osteonectin. Molecules of the SIBLING family, matrix metalloproteinases, and vascular and nerve mediators are also implicated in the formation of a reparative dentinal bridge, osteo/orthodentin closing the pulp exposure. Beneath a calciotraumatic line, a thin layer identified as reactionary dentin underlines the periphery of the pulp chamber. Inflammatory and/or noninflammatory processes contribute to produce a reparative dentinal bridge closing the pulp exposure, with minute canaliculi and large tunnel defects. Depending on the form and severity of the inflammatory and noninflammatory processes, and according to the capping agent, pulp reactions are induced specifically.

Background: After indirect capping, injured odontoblasts generate reactionary dentin, whereas after direct capping of a pulp exposure pulp, cells stimulate the formation of reparative dentin. The aim of this study was to evaluate and compare the effects of two direct capping agents on pulp tissue reactions: Hydrogel (a bovine serum albumin (BSA)/glutaraldehyde,) and Dycal (a calcium hydroxide-based capping agent). Methods: In 6-week-old male Sprague-Dawley rats, occlusal cavities were drilled in the first maxillary molars, and the pulps were exposed. In one of the groups, 24 right molars were capped with Hydrogel (G1), whereas in the other group 24 M were capped with Dycal (G2). After 1 to 4 weeks, the rats were anaesthetized intraperitoneally (six rats per group) and perfused intracardiacally with 4 % paraformaldehyde fixative. Maxillary molar's blocks were demineralized with a 4.13 % EDTA solution, embedded in paraffin, and the sections were histologically stained. Measurements of the thickness of reactionary dentin and area of inflammation were measured with ImageJ software. Results were compared with Kruskal Wallis and Mann Whitney U tests at p = 0.05. Results: One week after Dycal capping, a statistically significant large number of aggregates of pulp cells enlightened pulpal inflammation compared to Hydrogel. At 2-3 weeks, reactionary dentin formation was increased at the periphery of the pulp chamber. After 4 weeks, a dentinal bridge sealed partially the pulp exposure, while tunnel defects persisting across reparative osteodentin. In contrast, 1 week after Hydrogel capping, inflammation was barely detectable. Hydrogel induced the massive apposition of reactionary dentin at the pulp periphery, and reparative dentin was developing within the pulp. The degradation of Hydrogel releases glutaraldehyde acting on pulp cells as a fixative and consequently favoring BSA bioactivity. Conclusion: After Hydrogel capping, nemosis stimulates pulp mineralization, improving reactionary and reparative dentin formation. In contrast, the highly alkaline compound Dycal produced inflammation within the pulp. The differences between the two capping agents suggest that Hydrogel might present some clinical advantages over Dycal.