The presence of autophagy in human periapical lesions.

INTRODUCTION

Autophagy, a lysosome- or endosome-mediated self-degradation process, participates in diverse neurodegenerative diseases, cancer, and inflammatory diseases associated with apoptosis. This study aims to identify the presence of autophagy in human periapical lesions and its possible colocalization with apoptosis.

METHODS

Forty-seven samples of human periapical lesions diagnosed as radicular cysts (RCs, n = 23) or periapical granulomas (PG, n = 24) were examined. The inflammatory infiltrates of lesions were evaluated by hematoxylin-eosin staining, and the presence of autophagy was analyzed by immunohistochemistry using the autophagic marker LC3 antibody. Immunofluorescence and deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) double labeling was performed to colocalize LC3 with the apoptotic TUNEL signal. Transmission electron microscopy was conducted to assess the presence of autophagy.

RESULTS

LC3 was detected in all samples of RCs and PGs, but it was sparse in healthy dental pulp tissues. Macrophages, lymphocytes, polymorphonuclear leukocytes, and endothelial cells were stained positive for LC3 in both types of lesions. Epithelial cells were also stained positive for LC3 in RCs. Quantitative analysis revealed that LC3 expression in RCs is significantly greater than that in PGs. Immunofluorescence and TUNEL double-labeling analysis revealed that LC3 was partially colocalized with the TUNEL signal in both RCs and PGs. Furthermore, transmission electron microscopy confirmed the presence of autophagy and their partial colocalization with apoptotic nucleus at the ultrastructural level.

CONCLUSIONS

Our findings indicate that autophagy is present in clinical periapical lesions, which is partially associated with apoptosis.