On the repair of the dentine barrier

The overall aim of this thesis was to study some aspects of the repair of the dentine barrier, especially in conjunction with dental pulp capping. Understanding the events leading to the healing of the dentine and pulp, and hence successfully preserving the vitality and functions of the tooth, would lead to a scientific basis for a less invasive treatment of pulp exposures than performing root canal treatments. The surfaces of the body have physiological barrier functions aimed at protecting the body from external noxious agents. In the tooth, the odontoblasts, which line the outermost part of the pulp and are responsible for the formation of dentine, play a central role in the barrier function and thus in the defence mechanisms of the tooth. The micro-organisms in the caries lesion can reach the pulp via the dentinal tubules. However, the barrier function helps to prevent microbial invasion and thereby avoid deleterious inflammation and subsequent necrosis of the pulp. Dentine repair is an important part of the barrier function. There are however doubts as to whether the repair also leads to restitution of the function and the ability to withstand bacterial influx over the longer term. Pulp capping is a treatment method used when the pulp has been exposed in order to stimulate healing of the pulp and dentine. The evidence for repair of the dentine after pulp capping in humans has been studied by means of a systematic review. The focus of the literature search was studies performed in humans where hard tissue formation had been studied with the aid of a microscope. We concluded, based on the limited evidence available, that calcium hydroxide based materials but not bonding agents promote formation of a hard tissue bridge. Scientific evidence was lacking as to whether MTA was better than calcium hydroxide based materials in this regard. A gel (Emdogain Gel) containing amelogenin, known to be involved in dentinogenesis, was evaluated with regard to formation of hard tissue in a clinical study. A greater amount of hard tissue was formed after application of the gel compared to the control. Characterization of the tissue concluded it to be dentine, based on its content of type 1 collagen and dentine sialoprotein, although it was not formed as a continuous bridge covering the pulp wound. Beneath a deep caries lesion an important part of the barrier function is the odontoblasts' response to bacteria with the formation of new dentine. A cell model with odontoblasts was used to study the effects of clinical isolates from a deep carious lesion on their viability and production of type 1 collagen, the major component of the dentine in the early stages of its formation. There were bacteria that negatively affected the viability of the odontoblast-like cells and different bacteria varied in their effects on type 1 collagen production, suggesting that some bacteria may have a direct influence on the odontoblasts' ability to form dentine. In summary; Emdogain Gel initiated dentine formation, though not in a form that could constitute a barrier and there are indications that bacteria may differentially affect the odontoblasts' ability to repair the dentine barrier.