Host-mineral trioxide aggregate inflammatory molecular signaling and biomineralization ability

The biological processes underlying the ability of mineral trioxide aggregate (MTA) to promote hard-tissue deposition and wound healing remain unclear. To further study these processes, specific signaling molecules related to the inflammatory response and the biomineralization process were analyzed to assess host-MTA interactions in vivo.

For cytokine level quantification and immunohistochemical analysis, human dentin tubes were filled with ProRoot MTA (Dentsply, Tulsa Dental, OK) or kept empty and were implanted in subcutaneous tissues in the backs of mice. Dentin tubes were retrieved and subsequently observed using a scanning electron microscope.

MTA induced a time-dependent proinflammatory cytokine up-regulation up to 3 days. Immunohistochemical analyses showed an up-regulated expression of myeloperoxidase, nuclear factor-kappa B, activating protein-1, cyclooxygenase-2, inducible nitric oxide synthase, and vascular endothelial growth factor on day 1. Scanning electron microscopic examination revealed the presence of apatite-like clusters on collagen fibrils over the surface of tubes containing MTA. With the increase in time after implantation, a more extensive mineralization showing a compact layer of apatite was observed.

MTA induced a proinflammatory and pro-wound healing environment. The biomineralization process occurred simultaneously at the biomaterial-dentin-tissue interface, with the acute inflammatory response. This promoted the integration of the biomaterial into the environment.