Pathogenesis
Pathogenesis
In chronic pulpitis, the adaptive immune system plays a greater role than in acute disease. CD4+ T helper cells, CD8+ cytotoxic T cells, B cells, and plasma cells producing IgG, IgA, and IgM are characteristic. These cells release cytokines (IFN-γ, IL-4, IL-10) that modulate inflammation without resolving it.
Macrophages accumulate and engage in frustrated phagocytosis of persistent bacterial antigens. Mast cells degranulate, releasing histamine and tryptase. Fibroblasts proliferate and deposit collagen — explaining the fibrous pulp replacement seen histologically. Fibrous tissue has poor healing capacity and reduced pain sensation, explaining the minimal symptoms.
Pulp calcifications (pulp stones, diffuse calcifications) form through dystrophic mineralization in chronically inflamed, partially necrotic regions. Mineral deposits may be free-floating in the pulp chamber (true pulp stones with tubular structure) or attached to dentin walls (false stones without tubular structure).
In open chronic pulpitis with large carious exposures in young patients, the abundant blood supply from wide apical foramina supports formation of exuberant granulation tissue (pulp polyp) rather than necrosis. Epithelium from adjacent oral mucosa may migrate over the polyp surface over time.