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  • Title: Pulpal ischemia in man: effects on detection threshold, A-delta neural response and sharp dental pain.
    Author: Ahlquist M, Franzén O.
    Journal: Endod Dent Traumatol; 1999 Feb; 15(1):6-16. PubMed ID: 10219148.
    Abstract:
    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.
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