Hypersensitive dentine responds to normal changes in touch or temperat
ure with abnormal pain sensations. This paper reviews studies that hav
e 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-r
elated 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 n
erve terminals correlates with the pulpal gradients of nerve growth fa
ctor that have been demonstrated in normal teeth by in situ hybridizat
ion histochemistry. When shallow cavities are drilled into the outer d
entine of rat molars a five-to-eight-fold increase in pulpal nerve gro
wth factor precedes the extensive structural changes in the sensory ne
rve fibres in pulp and dentine near the injury. Those nerve growth fac
tor and sensory nerve reactions eventually subside if healing occurs,
but both continue if inflammation continues. Evidence correlating pulp
al inflammation with long-term changes in central trigeminal pain path
ways is reviewed. There can be extensive neuroplasticity after tooth i
njury, both within dental pain fibres and in central pain pathways. Th
e timing of those alterations of nerve structure, location, and cytoch
emistry is consistent with their involvement in mechanisms of dentine
hypersensitivity.