Direct pulp capping procedures - Evidence and practice

Abstract

The aim of direct pulp capping (DPC) is to promote pulp healing and mineralized tissue barrier formation by placing a dental biomaterial directly over the exposed pulp. Successful application of this approach avoids the need for further and more extensive treatment. In order to ensure a complete pulp healing with the placement of restorative materials, a mineralized tissue barrier must form to protect the pulp from microbial invasion. The formation of mineralized tissue barrier can only be induced when there is a significant reduction in pulp inflammation and infection. Consequently, promoting the healing of pulp inflammation may provide a favorable therapeutic opportunity to maintain the sustainability of DPC treatment. Mineralized tissue formation was observed as the favorable reaction of exposed pulp tissue against a variety of dental biomaterials utilized for DPC. This observation reveals an intrinsic capacity of pulp tissue for healing. Therefore, this review focuses on the DPC and its healing procedure as well as the materials used for DPC treatment and their mechanisms of action to promote pulpal healing. In addition, the factors that can affect the healing process of DPC, clinical considerations and future perspective has been described.

Keywords: Bioceramics; Calcium hydroxide; Direct pulp capping; Mineral trioxide aggregate; Pulp capping materials; Vital pulp therapy.

Fig. 1

Schematic representation of inflammatory response to bacterial penetration into the pulp tissue after exposure. After being exposed to carious lesions, the inflammatory response becomes more intense, and neutrophils and macrophages that have just come from blood vessels through diapedeses start to accumulate in the odontoblast layer. The layer of odontoblasts close to the infected dentine and the underlying pulp becomes necrotic, and bacteria penetrate into the pulp, causing inflammation in the entire pulp tissue.

Fig. 2

Schematic representation of the healing of dental pulp after exposure. Resolution of inflammation and tissue repair are achievable after the removal of invading microorganisms. The main components in these two processes are dental pulp stem cells and M2-polarized macrophages. Both of these cells release anti-inflammatory molecules that suppress inflammation and promote tissue healing. It is generally accepted that cell polarization towards the M1 or M2 phenotype is the mechanism through which macrophages are activated. They phagocytose bacteria, release pro-inflammatory cytokines, and initiate the immunological response.

Fig. 3

Schematic presentation of factors affecting DPC healing process. Pulp inflammation: various phases of inflammation of the pulp have been described, including mild, moderate, and severe inflammation; Operative debris: operative debris includes dentinal chips and foreign particles that can increase the activity of pulpal inflammatory cells and interrupt the dentin bridge integrity; Tunnel defects: the number of vessels injured during exposure and the severity of the pulp injury can both contribute to the tunnel defect, which can lead to microleakage that facilitates bacterial communication and recontamination. Incomplete dentin bridge formation: it might contain pulp tissue and can penetrate microorganisms.

Fig. 4

Graphical illustration of future perspective of DPC materials. Potential benefits might be obtained from combining bioactive molecules, or nanoparticles, or growth factors, or immunotherapy with future developments of currently existing DPC materials.