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Title: Understanding, modulating and mobilising natural dental repair
Author: De Carvalho Moreno Das Neves, Vitor
ISNI:       0000 0004 8500 347X
Awarding Body: King's College London
Current Institution: King's College London (University of London)
Date of Award: 2019
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Formation of tertiary dentine is a natural repair response to dentine damage. In tooth restoration following caries damage a number of new products in use are promoted as being "bioactive". These include substances such as MTA (mineral trioxide aggregate) (Dentsply), Biodentine® (Septodont), Dycal® (Dentsply). The main function of these compounds is to fill holes in the dentine but they are not formulated to specifically promote dentine formation. Although the repair is known to happen, a thorough and detailed understanding of the individual processes required for tissue repair, their initiation, inflammation cessation, cell differentiation and mineral secretion is clearly required in order to develop ways of promoting healing in situations where it is inefficient. This lack of clarity on what these materials do in the dental pulp led us to investigate and identify a pivotal pathway in the dental pulp (Wnt signaling) and cell types in vivo for stimulating natural tooth repair. Here we use a reproducible mouse molar damage protocol to confirm the knowledge obtained from stem cell research, to increase the reparative capacity of teeth without continuous growth, which are similar to the human teeth. The results showed that increasing local Wnt signalling via Wnt agonist drugs delivered on biodegradable collagen sponge after damage leads to increase of tertiary dentine formation in both reactionary and reparative dentinogenesis. Moreover, a finetuned genetic regulation, immunomodulation, and stem cell response controlled by proteins, growth factors and cytokines contribute to tertiary dentine formation.
Supervisor: Sharpe, Paul Thomas ; Grigoriadis, Agamemnon Emil Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available