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Updated: Mar 30, 2026

Development of a Direct Pulp-capping Model for the Evaluation of Pulpal Wound Healing and Reparative Dentin Formation in Mice
Published on: January 12, 2017
Dental Pulp Defence and Repair Mechanisms in Dental Caries
Jean-Christophe Farges1, Brigitte Alliot-Licht2, Emmanuelle Renard2
1Institut de Biologie et Chimie des Protéines, Laboratoire de Biologie Tissulaire et Ingénierie Thérapeutique, UMR 5305 CNRS, Université Lyon 1, 69367 Lyon, France ; Faculté d'Odontologie, Université de Lyon, Université Lyon 1, 69372 Lyon, France ; Hospices Civils de Lyon, Service de Consultations et de Traitements Dentaires, 69008 Lyon, France.
Abstract:
Dental caries is a chronic infectious disease resulting from the penetration of oral bacteria into the enamel and dentin. Microorganisms subsequently trigger inflammatory responses in the dental pulp. These events can lead to pulp healing if the infection is not too severe following the removal of diseased enamel and dentin tissues and clinical restoration of the tooth. However, chronic inflammation often persists in the pulp despite treatment, inducing permanent loss of normal tissue and reducing innate repair capacities. For complete tooth healing the formation of a reactionary/reparative dentin barrier to distance and protect the pulp from infectious agents and restorative materials is required. Clinical and in vitro experimental data clearly indicate that dentin barrier formation only occurs when pulp inflammation and infection are minimised, thus enabling reestablishment of tissue homeostasis and health. Therefore, promoting the resolution of pulp inflammation may provide a valuable therapeutic opportunity to ensure the sustainability of dental treatments. This paper focusses on key cellular and molecular mechanisms involved in pulp responses to bacteria and in the pulpal transition between caries-induced inflammation and dentinogenic-based repair. We report, using selected examples, different strategies potentially used by odontoblasts and specialized immune cells to combat dentin-invading bacteria in vivo.
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