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The odontoblast cell is responsible for forming primary dentine during tooth development, the more slowly deposited secondary dentine throughout the life of the tooth, and, when ‘irritated’, tertiary dentine in the pulp tissue adjacent to the source of challenge [31]. Dependent on the stimulant severity, tertiary dentine deposition can be either reactionary or reparative (Figure 2.1) [32]. Reactionary dentine is formed by an upregulation of existing odontoblast activity when the dentine–pulp complex is exposed to a relatively mild stimulus (e.g. shallow or slowly progressing carious disease process), whilst reparative dentine is formed generally after a stronger stimulus has led to odontoblast cell death (e.g. deep caries or traumatic exposure) [32, 33]. At a cellular level, reparative dentine is believed to be produced following cytodifferentiation of pulpal progenitor cells (DSPCs or other progenitor cells) and the formation of a new generation of odontoblast‐like cells [1, 32, 33]. Although this description of reparative dentinogenesis represents the currently accepted theory, others have highlighted the influence of other cells such as fibroblasts or fibrocytes as secretory cells [34, 35]. The cellular differentiation is guided by the influence of growth factors and other bioactive molecules released from both the dentine matrix and the pulp cells themselves [36, 37]. Whilst for didactic purposes the processes of reactionary and reparative dentinogenesis are considered separately in the event of pulp exposure, both are likely to occur simultaneously [38].

Figure 2.1 Schematic representation of the reparative process after pulp exposure, vital pulp treatment, and the potential influence of the material.

Inflammation is also an important stimulus that drives the reparative process [39], with odontoblasts involved in initial sensory stimulus transmission from the dentine and possessing an immunocompetent role in cellular defence [40]. Indeed, the low‐level release of inflammatory mediators such as interleukins‐2 and ‐6 in mineralizing cells in contact with an HCSC such as mineral trioxide aggregate (MTA) supports the need for a degree of inflammation in promoting regenerative processes [41].

A wide range of bioactive dentine matrix components are ‘fossilized’ in the mineralized tissue and released into the pulp during caries or trauma [38, 42]. Demineralization of dentine, and indeed contact with materials such as MTA [43], calcium hydroxide [44], and other agents [45], releases a plethora of bioactive molecules, including members of the transforming growth factor‐β (TGF‐β1) superfamily, which can stimulate a complex cascade of molecular events that promote pulp repair [36, 44]. These materials liberate dentine matrix components to varying degrees, highlighting the influence of the material in the biological response [46].

Using biologically based dental materials that promote the healing process is paramount in VPT [47]. Other strategies using irrigants to enhance the release of bioactive molecules from dentine in order to improve wound repair are also being developed [48]. Over the last 10 years, HCSCs have shown superior histological response compared with the gold‐standard material, calcium hydroxide, in VPT [9, 49]. HCSCs work in a similar way to calcium hydroxide but are more efficient in their interaction with dental pulp cells and dentine extracellular matrix (dECM) [50]. In reality, both their mechanisms of action remain nonspecific and untargeted in nature (Figure 2.1) [49, 51].