Host-mineral trioxide aggregate inflammatory molecular signaling and biomineralization ability.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Reyes-Carmona
Jessie F
JF
Postgraduate Dentistry Program of the Federal University of Santa Catarina, Florianópolis, SC, Brazil. jessreyesc@hotmail.com
Santos
Adair S
AS
Figueiredo
Claudia P
CP
Baggio
Cristiane H
CH
Felippe
Mara C S
MC
Felippe
Wilson T
WT
Cordeiro
Mabel M
MM
D017607:Aluminum Compounds / Q000494:pharmacology*; D000818:Animals; D001031:Apatites / Q000032:analysis; D002113:Calcification, Physiologic / Q000187:drug effects*; D017610:Calcium Compounds / Q000494:pharmacology*; D003094:Collagen / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000187:drug effects; D003804:Dentin / Q000648:ultrastructure; D004338:Drug Combinations; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000187:drug effects; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000187:drug effects; D009504:Neutrophils / Q000473:pathology; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D010087:Oxides / Q000494:pharmacology*; D009195:Peroxidase / Q000187:drug effects; D012387:Root Canal Filling Materials / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects*; D017640:Silicates / Q000494:pharmacology*; D040521:Subcutaneous Tissue / Q000187:drug effects; D013997:Time Factors; D018808:Transcription Factor AP-1 / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000187:drug effects
D017607:Aluminum Compounds; D001031:Apatites; D017610:Calcium Compounds; D004338:Drug Combinations; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D016328:NF-kappa B; D010087:Oxides; D012387:Root Canal Filling Materials; D017640:Silicates; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C086631:mineral trioxide aggregate; C467480:vascular endothelial growth factor A, mouse; D016753:Interleukin-10; D003094:Collagen; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2