Pathogenesis
Pulp inflammation follows classic inflammatory pathways but is complicated by the rigid dentin enclosure — the pulp cannot expand, leading to increased intrapulpal pressure.
Bacterial toxins stimulate pulp macrophages, mast cells, and dendritic cells to release inflammatory mediators including PGE2, bradykinin, histamine, and cytokines.
Vasodilation and increased vascular permeability cause edema, but the rigid pulp chamber prevents edema resorption, raising intrapulpal pressure.
This pressure compromises local blood flow, creating zones of ischemia and necrosis. Neuropeptides (substance P, CGRP) sensitize C-fibers and A-delta fibers, lowering pain thresholds.
In irreversible pulpitis, the inflammatory process is too advanced for the pulp to recover; without treatment, pulp necrosis is inevitable.