Preferential blocks of peripheral nerves have shown that myelinated nerves are more susceptible to local compression and less resistant to
asphyxia than unmyelinated fibers. Since two groups of functionally different nociceptors exist in the dental pulp, it is of theoretical and clinical interest to determine the influence of
ischemia on the sensitivity of human dental pulp, using standard means for testing tooth vitality and at the same time investigating the intensity coding in one pathway of the afferent trigeminal system.
Adrenaline was used to study the differential effect of
adrenaline-induced
ischemia on intradental A-delta nerve activity (INA) and the concomitant sharp
pain, as well as on the detection threshold for monopolar electrical stimulation. Cold (
ethyl chloride) and heat (heated
gutta-percha) stimulation was applied to the tooth surface. In accordance with the hydrodynamic theory of
dentin sensitivity the rapid fluid flow induced in the dentinal tubuli by these thermal stimuli is an adequate stimulus for selectively activating the A-delta nerves in healthy pulps. Consistency plots of the magnitude of the perceptual experience of sharp
pain against the neural population response in linear coordinates yielded a high product-moment correlation, implying linearity for the intensity coding relationship. In contrast to the significant reduction of INA and its perceptual correlate of sharp
pain after
adrenaline administration, the electrical detection threshold remained constant during the full test period, suggesting that electrical threshold measurements have their limitations as a diagnostic tool or criterion for assessing the sensitivity of the dental pulp. The absence of A-delta activity was parallelled by no sensation of sharp
pain. These findings suggested that the integrated neural A-delta activity constituted the underlying peripheral neurophysiological mechanism of the sensory intensity of sharp dental
pain.