Diclofenac exerts local anesthetic-like actions on rat masseter muscle afferent fibers.

The use of topical non-steroidal anti-inflammatory drugs, such as diclofenac, for the treatment of temporomandibular disorders-related myofascial pain is based on the premise that their analgesic effect is mediated by a local action on the excitability of muscle nociceptors, despite a lack of muscle inflammation in these patients. To investigate if diclofenac has an effect on muscle afferent fibers in the absence of inflammation, in vivo recordings of the response of masseter muscle afferent fibers to mechanical and noxious chemical (hypertonic saline) stimulation were made in anesthetized Sprague-Dawley rats. It was observed that injection of diclofenac (0.1 or 1 mg/ml) alone could elevate afferent mechanical threshold for a 10 min period post-injection. Hypertonic saline-evoked afferent discharge was also significantly attenuated by the higher concentration of diclofenac and lidocaine (20 mg/ml), but not by the lower concentration of diclofenac. Additional experiments were undertaken to investigate whether activation of ATP-sensitive potassium (K ATP) channels could contribute to the effects of diclofenac. The K ATP channel opener pinacidil (0.1 mg/ml) significantly enhanced potassium chloride-evoked afferent discharge consistent with the concept that masseter afferent fibers have functional K ATP channels, however, subsequent experiments indicated that diclofenac (1 mg/ml) significantly suppressed potassium chloride-evoked afferent discharge and that pinacidil did not affect hypertonic saline-evoked afferent discharge. These results indicate that diclofenac can exert a "local anesthetic-like" action on masseter afferent fibers in the absence of inflammation, but that this effect does not appear to involve the opening of K ATP channels.