Journal of Oral Microbiology · Published 2026-02-17 · DOI 10.1080/20002297.2026.2622207
Background Pulpitis is a common dental disease driven by complex microbial infections, yet its microbial origins, diversity, and pathogenic mechanisms remain incompletely understood. A major clinical challenge is the absence of objective biological criteria to assess the severity and reversibility of pulpal inflammation, which is essential for decision-making in vital pulp therapy (VPT).Objective This review aims to synthesize current evidence on the microbial landscape of pulpitis and to explore microbial- and host-derived biomarkers that may enable objective assessment of inflammation severity and support precision VPT.Design We comprehensively reviewed microorganisms implicated in pulpitis and their distinct virulence mechanisms underlying inflammatory responses and tissue damage. Particular emphasis was placed on host responses of dental pulp stem cells (DPSCs) to different microbial infections. Biomarker candidates reported across multiple studies were summarized, and single-cell transcriptomic evidence was integrated to validate microbe-specific DPSC responses.Results Distinct microorganisms associated with pulpitis exhibit heterogeneous virulence strategies, inducing diverse inflammatory and degenerative processes within the dental pulp. DPSCs display infection-specific transcriptional responses, revealing molecular signatures linked to inflammation severity and tissue repair potential. Emerging biomarkers derived from both microbial factors and host responses show consistency across studies, with single-cell analyses providing high-resolution validation of these microbe-specific patterns.Conclusions Microbial- and host-derived biomarkers hold significant translational potential for stratifying pulpitis severity, informing VPT decision-making, and predicting treatment prognosis. Integrating microbial characterization with host response profiling may advance objective diagnosis and personalized management of pulpitis.
Abstract from DOAJ. Public domain (CC0 1.0).
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