Exploring the Painless Nature and Potential Mechanisms of Asymptomatic Irreversible Pulpitis: A Narrative Review
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 endog...
| Main Authors: | , , |
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| Format: | ARTÍCULO |
| Language: | es_ES |
| Published: |
2024
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| Subjects: | |
| Online Access: | http://dspace.ucuenca.edu.ec/handle/123456789/44454 https://opendentistryjournal.com/VOLUME/18/ELOCATOR/e18742106281444/FULLTEXT/ |
| Summary: | 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. |
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