Effect of alpha7 nAChR-autophagy axis of deciduous tooth pulp stem cells in regulating IL-1beta in the process of physiological root resorption of deciduous teeth.

Physiological root resorption of deciduous teeth is a normal phenomenon occurring during the developmental stages of children. Previous research has indicated the pivotal role of the inflammatory microenvironment in this process, although the specific mechanisms remain unclear. This study is aimed at elucidating the involvement of the alpha7 nicotinic acetylcholine receptors (alpha7 nAChR)-autophagy axis in the regulation of the inflammatory microenvironment during physiological root resorption in deciduous teeth. Samples were collected from deciduous teeth at various stages of physiological root resorption, and deciduous dental pulp stem cells (DDPSCs) were isolated and cultured during the mid-phase of root resorption. The findings revealed a substantial infiltration of the pulp of deciduous teeth at the mid-phase of root resorption, characterized by elevated expression levels of alpha7 nAChR and IL-1beta. Significantly increased IL-1beta and alpha7 nAChR expressions were observed in DDPSCs during the mid-phase of root resorption, with alpha7 nAChR demonstrating a regulatory effect on IL-1beta. Moreover, evidence suggested that mechanical stress may act as a trigger, regulating autophagy and IL-1 expression via alpha7 nAChR. In conclusion, mechanical stress was identified as a regulator of autophagy in DDPSCs through alpha7 nAChR, influencing the expression of IL-1beta and contributing to the formation of the inflammatory microenvironment. This mechanism plays a crucial role in the physiological root resorption of deciduous teeth. KEY MESSAGES: The pulp of deciduous teeth at mid-phase of root resorption was heavily infiltrated with high expression of alpha7nAChR and IL-1beta. alpha7 nAChR acts as an initiating factor to regulate IL-1beta through autophagy in DDPSCs. Mechanical stress can regulate autophagy of DDPSCs through alpha7 nAChR and thus affect IL-1beta expression and inflammatory microenvironment formation in physiological root resorption in deciduous teeth.