Pulpal Reaction to Caries

The dental caries may be in any form or at any site, affects the underlying pulp. The initiation of pulpal inflammation also stimulates the repair process. A balance usually occurs between repair and injury and deviation from the balance lead to changes in the dentin-pulp complex.

The cellular injury associated with caries arises from acidic environment created by diffusion of bacterial acids. The ability of the cells to withstand this acid environment depends upon hydrogen ion concentration. Local lymphatic drainage in the pulp may contribute to clearance of acid but the pulpal lymphatic system is not well developed. The odontoblasts are significantly reduced in size beneath the active enamel lesions whereas at the site of arrested lesions such reduction is not exhibited. Before the carious lesion reaches dentino-enamel junction, a significant reduction in cytoplasm to nucleus ratio of odontoblasts and also reduction in predentin thickness is observed. At ultrastructural level increase in activity of phosphate enzyme is reported in odontoblasts and in predentin beneath

the carious lesions.

The terms ‘slight’, ‘moderate’ and ‘severe’ have the subjectivity and also the varied interpretation of the histopathological results make it difficult to standardize the classification of pulpal reactions.

The onset of pulpal reactions to caries starts early, but its effect has not been documented properly. Pulpal reactions have been established even with the formation of white-spot lesions. There are marked changes in dentin with 'acute' or rapidly progressing caries than with ‘arrested’ or slow progressing caries. The odontoblasts in active lesion were significantly smaller than were, odontoblasts in other lesions. The cellular proliferation of the cell free zone is also observed in active lesion only. Changes in the sub-odontoblastic region also occur early and these changes might include early onset of neurogenic inflammatory reactions.

The active lesions do not show any marked changes in dentin mineralization. Slowly the demineralization of the affected dentin starts. Soon after the demineralization, the evidence of tertiary dentin can be noted at the pulp dentin border usually defined as reactionary dentin. The pulp adjacent to deep caries

show the presence of chronic inflammatory exudates, including lymphocytes, macrophages and plasma cells. The localized increase in dentin thickness is often accompanied by reduced odonotoblastic layer in the affected area. The tertiary dentin can be seen at the affected site. The accumulation of inflammatory cells is particularly great whenever the bacteria associated with caries process reach the

tertiary dentin. This stage corresponds to severe pulpal inflammation with minimum chances of healing. It may lead to pulp necrosis at a later stage.

In case of rampant caries, the breakdown of affected enamel and dentin will occur within months. This leads to destruction of odontoblasts and lack of tertiary dentin formation. If the odontoblasts are destroyed slowly, there is formation of hard tissue, which is initially atubular with some cellular inclusions, defined as fibrodentin and interface dentin. The progress of caries, if halted, lead to formation of reparative dentin with differentiation of new secondary odontoblast like cells. If the lesion is allowed to progress, pulp necrosis may follow.

The immune system helps in defence mechanism of pulp. In association with carious dentin, accumulation of immuno-competent cells has been demonstrated. During rapid lesion progression, accumulation of immuno-competent cells is observed in conjunction with reduced number of primary odontoblasts. In case the tertiary dentin develops, it is formed as an atubular dentin.