Molecular mediators of pulp inflammation and regeneration

Abstract

Dental tissue infection results in immune and inflammatory responses mediated by molecular and cellular events that, if unchecked, result in tissue breakdown. The tooth, like other tissues and organs within the body, will attempt to repair and regenerate its own hard and soft tissues given the appropriate conditions and environment. However, unchecked infection and inflammation will have a significant impact on the natural regenerative responses of the dental tissues. Thus far, there have been limited studies addressing the inter‐relationship between these two processes, which are clearly linked by molecular and cellular events. Indeed, locally derived growth factors, cytokines, and chemokines, which are all sequestrated within the dental tissue extracellular matrix and are also expressed by pulpal cells, immune cells, and/or necrotic host tissue, will have considerable impact on the cellular events within the tissue. In addition to the molecular signaling, there will be important cellular interactions that will occur as stem cells, resident or recruited to the pulp, have known immuno‐modulatory activity with significant implications for regenerative events. In this review, we aim to explore how the pulpal tissue responds to the invading bacteria and the signaling mechanisms that are now being described and are important in regulating both the immune/inflammatory and regenerative responses.

Tooth whitening: From the established treatments to novel approaches to prevent side effects

“…Thus, molecular mechanisms underlying clinical dental pain and hypersensitivity remain uncertain. Many molecular candidates have been proposed as mediators of this problem . Tooth hypersensitivity after whitening treatments probably occurs as a consequence of the functional properties of the chemosensitive ion channel called TRPA1 (transient receptor potential channel with ankyrin domain‐type 1) .…”

“…Many molecular candidates have been proposed as mediators of this problem. 121 Tooth hypersensitivity after whitening treatments probably occurs as a consequence of the functional properties of the chemosensitive ion channel called TRPA1 (transient receptor potential channel with ankyrin domain-type 1). 122 This ion channel is associated with the pain caused by oxidants, including hydrogen peroxide.…”

Scaffolds to Control Inflammation and Facilitate Dental Pulp Regeneration

“…Initially inflammatory mediators are critical drivers of the repair process and stimulate reparative dentin formation by odontoblasts and the differentiation of progenitor cells into a repair phenotype (6, 34, 35). If expression of these mediators persists however, inflammation becomes sustained in the pulp, creating a maelstrom of cytotoxic and tissue disrupting effects ultimately leading to tissue necrosis (8, 29, 31, 32, 36, 37). …”

“…Sustained pulpal inflammation not only damages the pulp tissue, but also actively prevents the repair response by down-regulating the recruitment and differentiation of mesenchymal progenitor cells (8, 29, 31, 32). Macrophages play a pivotal role in the innate immune response, and it is now well-established that they are capable of responding to various complex stimuli, by polarizing into either pro-inflammatory (M 1 ) or pro-resolution (M 2 ) phenotypes, with many subtle variations on these two broad classifications (43–46).…”

Response to Dr. Tjäderhane and Dr. Salo's letter

“…These findings perhaps emphasize the importance of characterizing the temporal expression profiles of candidate molecules when elucidating the responses of odontoblasts and pulp cells to bacterial challenge during caries progression. It is becoming increasingly clear that a complex interplay exists between inflammatory and regenerative processes during caries progression (reviewed in Smith et al 2012, Cooper & Smith 2013. A deeper understanding of this complex interplay will provide an important foundation upon which to base the future clinical translation of regenerative endodontics.…”