Implications of inflammasomes in dental pulp inflammation: immunopathology and therapeutic targeting.

Abstract

Pulpitis is a dynamic condition that affects vascular and immune responses. A major driver of inflammation is the inflammasome, which regulates interleukin-1 (IL-1) family cytokines and pyroptosis. Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) activate the inflammasome via caspase recruitment, which is essential for the inflammasome's immunomodulatory effects. In order to synthesize evidence for this review, a comprehensive search was conducted in PubMed, Scopus, and Web of Science. Subsequently, preclinical models and clinical studies on the role of inflammasome components in dental pulp inflammation were selected and critically presented. According to recent research, factors associated with the inflammasome are dysregulated during dental pulpitis, while therapeutic targeting through computational discovery of anti-inflammasome ligands and cell-free exosome-based treatments can counteract the immunopathology of dental pulpitis. Although preclinical studies were promising, comprehensive clinical trials of IL-1 family and inflammasome inhibitors are required for translating current research into viable treatments for patients with dental pulpitis. Future work should prioritize clinical validation to enable implementation in patient care.