In addition, NLRP3 activation induces the release of secondary mediators such as prostaglandin E2 (PGE2) and TNF-α, which exacerbate inflammation and sensitize nociceptors including transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, and acid-sensing ion channel 3, thereby promoting hyperalgesia in pulpitis [50,52]. This evidence concerns the gene NLRP3 and pulpitis.