Objectives: Molecular mechanisms regulating inflammatory process in periapical lesions after root canal treatment (RCT) are still poorly understood. The aim of this study is to profile gene expression patterns in rat periapical lesions after RCT. Methods: Periapical lesions were induced experimentally by exposing the pulp in the lower first molars of Sprague-Dawley rats (male, 10-weeks). Three weeks after developing the lesions, the animals received or did not receive root canal filling (RCF), and were sacrificed 1 and 4 weeks after that. The periapical lesions were assessed histologically and radiographically. After periapical tissues were harvested, the total RNA was extracted and processed for DNA microarray analysis representing approximately 30,000 genes. Data analysis was performed using GeneSpring software. Genes showing remarkably different expression in microarray were confirmed by real-time PCR. Results: Histological and radiographical images showed that lesions expanded dramatically 3 weeks after exposing the pulp (severe inflammation) and stabilized 4 weeks after RCF (healing). In the 30,000 genes on the array 203 genes were up-regulated by over 5-fold (IL-1&beta, MMP-12, PDGF-&alpha, etc.) and 864 genes were down-regulated by 20% or more (Cathepsin E, Caspase 8, Calmodulin 3, etc.) in the severe inflammation compared to the healthy control, in contrast, 133 genes were up-regulated by over 5-fold (IL-1&alpha, MMP-3, Integrin &beta6, etc.) and 50 genes were down-regulated by 20% or more (Mast cell protease 9, Defensin-NP3 precursor, Defensin-&alpha, etc.) in the healing phase compared to the severe inflammation. Several genes were verified by real-time PCR. Conclusions: The present study demonstrated a global view of the genes regulated in developing and healing of periapical inflammation. These findings provided a useful basis for screening candidate genes for diagnosis inflammatory and healing process in the periapical lesion during RCT.

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