Sodium acetylsalicylate and the role of prostaglandins in the mechanism of intradental pain.

In order to study the effect of sodium acetylsalicylate and the role of prostaglandins on intradental nerve impulse activity experiments were performed on the teeth of anaesthetized cats. Nerve impulse activity was induced by mechanical and chemical stimuli and recorded by means of electrodes inserted into dentinal cavities. It was shown that such activity could not be blocked by sodium acetylsalicylate or indomethacin given locally or i.v. PGE2 failed to excite the sensory units when given locally (3.5 microng/ml) or intraarterially (35-140 ng/min) alone or in combination with mechanical and thermal stimuli or combined with local application of histamine (10 mg/ml) or bradykinin (10 mg/ml). Intraarterial infusion or arachidonic acid, a precursor to PGE2, PGF2 alpha PGG2 and PGH2 failed to change the excitability even on applying local stimuli to the pulp or with local application of histamine or bradykinin. These findings seem to indicate that the increased sensitivity of the tooth to thermal stimuli seen during acute pulpitis is not due to formation of prostaglandins.