2. Pathogenesis of pulpitis resulting from dental caries

Demonstrable evidence suggests that the pattern of inflammation in the tooth affected by carious attack is determined by the permeability of dentin and the proximity of the carious lesion to the pulp. Accumulation of immunologically competent chronic inflammatory cells either accompanies or follows retrogressive changes in the odontoblast layer beneath the lesion. Deposition of collagen and proliferation of small vessels are also features of early inflam matory changes in the pulp. A transition from a chronic to an acute inflammatory reaction occurs as the lesion approximates the pulp or invades reparative dentin. Progressive accumulation of large numbers of neutrophils, presumably drawn by chemotactic influences, results in suppuration that may be diffuse or may become localized to form an abscess. Surface ulceration may develop as a result of chronic suppuration, which remains confined to the areas of the pulp beneath the carious lesion, and results in the creation of a space. In slow progressing lesions, continued formation of reparative dentin may be capable of preventing pulp exposure. Degeneration of the pulp occurs when the number of bacteria entering the pulp exceeds the ability of the blood vessels of the pulp to furnish a sufficient number of blood leukocytes to repel the bacteria. Hyperplastic pulpitis represents a proliferation of chronic inflammatory tissue in response to carious exposure to the young pulp.