Neurogenic Inflammation Pathway on the Up-Regulation of Voltage-Gated Sodium Channel NaV1.7 in Experimental Flare-Up Post-Dental Pulp Tissue Extirpation

Dental caries is one of infectious diseases that still has a serious problem and causes irreversible pulpitis. In endodontic treatment, pain or swelling can occur immediately during the treatment in the root canal of teeth. This study aimed to explain the role of neurogenic inflammation and immunology in the occurrence of post-root canal flare-ups based on the vitality of pulp tissue and the expression of CGRP, NaV1.7 in nerve cells, and HSP70 in macrophages. The experimental study was conducted to the 15 Sprague Dawley rats divided into three groups: the control group, pulp tissue extirpation group, and LPS group. The pulp tissue was extirpated, and the collected samples were obtained from the apical field of the mandibular incisor. Examination was done with immunohistochemical methods. Significant differences were found in NaV1.7, HSP70, and NaV1.7 expressions. The expression of CGRP and HSP70 experienced a significant increase while the expression of Nav1.7 experienced a significant decrease. The extirpation of the pulp tissue increased the expressions of CGRP, HSP70, and NaV1.7 in the pulp tissue. Increased CGRP in nerve cells and HSP70 in macrophage cells could enrich TNF, thereby causing NaV1.7 to increase. An increase in CGRP can directly incline NaV1.7 through the AC and PLC pathways. The administration of LPS followed by the pulp tissue’s extirpation causes over-expression of HSP70, which will inhibit TRAF6. Consequently, it decreases TNF, which then decline NaV1.7