Exploring the Painless Nature and Potential Mechanisms of Asymptomatic Irreversible Pulpitis: A Narrative Review

Author:

Cabrera-Abad Daniela Paola,Jara-Vergara Verónica Cristina,Álvarez-Vásquez José Luis

Abstract

Background Considering the extensive innervation of the pulp tissue, asymptomatic irreversible pulpitis (AIP) or “silent pulpitis” represents a confounding clinical condition. Previous studies have attributed the painless nature of AIP to the inhibition of pulpal nociceptors by local endogenous analgesics. However, there is a lack of recent information concerning its painless nature, and paradoxically, patients with dental pain are diagnosed with AIP daily worldwide. In addition, no recent review has explored the potential AIP-related mechanisms. Objective This narrative review aims to explore and update the potential mechanisms involved in the painless nature of AIP to improve our current understanding of the asymptomatic character of this clinical condition. Methods An electronic search was performed in the PubMed and Scopus databases, using as search terms “asymptomatic irreversible pulpitis,” “dental pulp,” “endogenous opioids,” “endogenous cannabinoids,” “somatostatin,” “GABA,” “bombesin,” “cortistatin,” “galanin,” and “specialized pro-resolving lipid mediators.” Results Endogenous opioids, G protein-activated inwardly rectifying K+ channels, endogenous cannabinoids, γ-aminobutyric acid, and neuropeptides (i.e. somatostatin, cortistatin, galanin, and bombesin) could be involved in AIP-related analgesia. Additionally, specialized pro-resolving lipid mediators, such as lipoxins, resolvins, maresins, and protectins, as well as oxytocin, phoenixin, opiorphin, and adipokines, could also be involved in this clinical condition. Conclusion This narrative review provides updated information on the potentially involved mechanisms in AIP. Nevertheless, the precise mechanisms responsible for the lack of symptoms in AIP remain to be elucidated, and further research is warranted.

Publisher

Bentham Science Publishers Ltd.

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