Etiology
Etiology
Slowly progressing deep caries is the predominant cause. The gradual advancement of the carious lesion allows the pulp to mount adaptive defensive responses — tertiary dentin deposition, immunological tolerance — while simultaneous low-level damage accumulates. The pulp-dentin complex essentially 'races' to wall off the approaching infection.
Chronic pulpitis may follow incompletely resolved acute pulpitis — either because the stimulus was reduced but not eliminated (e.g., partial caries removal, inadequate restoration) or because the initial acute episode exceeded the pulp's healing capacity.
Recurrent caries beneath existing restorations, microleakage at restoration margins, and progression of cracks in teeth provide pathways for slow, sustained antigen delivery that characterizes chronic inflammation. Periodontal-endodontic lesions where periodontal bacteria access lateral canals represent a less common but important etiology.