Estrogen deficiency aggravates apical periodontitis by regulating NLRP3/caspase-1/IL-1β axis.

Estrogen plays critical roles in apical periodontitis and subsequent bone loss, however the mechanism is not clear yet. In this study, we aimed to study the underlying mechanism of estrogen in apical periodontitis using both clinic samples and animal model. Clinically, as estrogen physiologically declines in elder female patients (premenopausal verses postmenopausal patients), we found that the expression level of NLRP3/Caspase-1/IL-1β signaling pathway was elevated in the infected apical tissues of postmenopausal patients as compared to the premenopausal patients, suggesting that this pathway is involved in the estrogen-mediated apical periodontitis. Furthermore, by analyzing the well-established OVX (estrogen deficiency model) animal model, we confirmed that the expression level of NLRP3/Caspase-1/IL-1β signaling pathway was also elevated in the infection areas of apical periodontitis in OVX animals. Importantly, as the periodontitis progressed, the subsequent bone loss was aggravated significantly. Thus, taken all these data together, our results demonstrated that the NLRP3/Caspase-1/IL-1β signaling pathway is involved in the estrogen-mediated apical periodontitis and the consequent bone loss in both human being and animal model. This study may provide a potential target for female apical periodontitis therapy. AJTR