Year: 2015
Type: review
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.
Source: Mediators of Inflammation
DOI: 10.1155/2015/230251
Institutions: Lyon 1 Université, Centre National de la Recherche Scientifique, Université de Lyon, Institut de Biologie et de Chimie des Protéines, Hospices Civils de Lyon, Laboratoire de Biologie Tissulaire et d'Ingénierie Thérapeutique, Inserm, Center for Research in Transplantation and Translational Immunology, Université de Nantes, Nantes Université, University of Birmingham
Language: English
Subfield: Oral Surgery
Field: Dentistry
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,943
OpenAlex ID: W2168535055
