Local anesthesia does not block mustard-oil-induced temporomandibular inflammation.

Abstract

Temporomandibular joint (TMJ) disorders and rheumatoid arthritis are two conditions in which neurogenic mechanisms may play a critical role. We investigated the neurogenic contribution underlying acute TMJ inflammation by evaluating effects of local anesthetic blockade of afferent innervation on the development of mustard oil (MO)-induced edema in the rat TMJ area. Groups of eight adult male Sprague-Dawley rats were anesthetized by intraperitoneal alpha-chloralose and urethane. A saline injection into the right TMJ followed by MO (1% to 60%) 6 min later elicited dose-dependent edema development (P < 0.05, repeated measures analysis of variance). Lidocaine (5%) or bupivacaine (0.5%) followed by MO (1% or 40%) did not produce edema development different from saline controls (P > 0.05, repeated measures analysis of variance). The failure of local anesthetic blockade to prevent MO-induced edema is not consistent with MO acting through a neurogenic mechanism, as traditionally perceived. Inflammation found in temporomandibular disorders and rheumatoid arthritis may result from mediators released by pain-sensing neurons. Local anesthesia failed to block simulated neurogenic temporomandibular inflammation in a rat model, suggesting that functional neuronal input may not be necessary for the promotion of inflammation.