Dynamic plasticity of dental sensory nerve structure and cytochemistry.

Hypersensitive dentine responds to normal changes in touch or temperature with abnormal pain sensations. This paper reviews studies that have shown dynamic changes in sensory nerve structure, cytochemistry and location after tooth injury, suggesting that those changes contribute to dentine hypersensitivity. Nerve fibres containing calcitonin gene-related peptide (CGRP) are the main type of sensory fibre to innervate dentine. Evidence that many of those dentinal nerve endings originate from small myelinated fibres is presented here. The location of CGRP nerve terminals correlates with the pulpal gradients of nerve growth factor that have been demonstrated in normal teeth by in situ hybridization histochemistry. When shallow cavities are drilled into the outer dentine of rat molars a five-to-eight-fold increase in pulpal nerve growth factor precedes the extensive structural changes in the sensory nerve reactions eventually subside if healing occurs, but both continue if inflammation continues. Evidence correlating pulpal inflammation with long-term changes in central trigeminal pain pathways is reviewed. There can be extensive neuroplasticity after tooth injury, both within dental pain fibres and in central pain pathways. The timing of those alterations of nerve structure, location, and cytochemistry is consistent with their involvement in mechanisms of dentine hypersensitivity.