Capsaicin-induced Joint Inflammation Is Not Blocked by Local Anesthesia. DISCUSSION

In: Health

9 Sep 2009

Local Anesthesia

The application of capsaicin to the rat TMJ region resulted in an inflammatory reaction illustrated by the expansion of the periarticular tissue and plasma extravasation as demonstrated by Evan’s blue dye staining in this area of interest. Since capsaicin binds to VR1 receptors located on primary sensory afferents innervating the rat TMJ region to produce edema and plasma extravasation, the findings in this study suggest that acute inflammation of the rat TMJ region encompasses a neurogenic component. In addition, sustained and reversible increase in ipsilateral masseter and digastric muscle activities were evoked with the deposition of capsaicin into the rat TMJ region.

Subsequently, to understand the characteristics of the potential neurogenic mechanism in the development of acute inflammation in the TMJ region evoked by capsaicin, the evaluation of the consequences of nerve conduction inhibition was performed. Although a complete blockade of nerve conduction was confirmed with the lack of EMG response to capsaicin, the amount of edema and plasma extravasation generated by the application of different concentrations of capsaicin did not significantly differ among the saline pretreated and bupivacaine pretreated rats. Thus, this present study also demonstrated that the administration of local anesthetic prior to the injection of capsaicin failed to significantly reduce the resultant tissue expansion and plasma extravasation in the TMJ region; however, the reflex jaw muscle activity was abolished. Need medication you can’t afford? Buy levitra professional canada

The plasma extravasation induced by capsaicin administration in the rat TMJ region suggests a neurogenic component in its inflammatory process; however, the absence of a significant reduction in capsaicin-induced edema in the local anesthetic pretreated TMJ region questions the true mechanism underlying neurogenic inflammation and the pure neurogenic nature of the inflammatory irritant, capsaicin. The findings from this investigation suggest 2 possible interpretations. First, capsaicin may evoke the direct release of inflammatory mediators from neuronal terminals without the conduction of action potentials along the axon. Alternatively, capsaicin may predominantly act in a nonneurogenic fashion when applied to the TMJ region due to its inherent inflammatory nature or the activation of VR1 receptors located on other cellular components. Cialis super active

In the event that capsaicin is indeed purely acting in a neurogenic fashion, the lack of the necessity for nerve conduction disproves both the classical and current concepts of neurogenic inflammation. Past studies have argued that the axon reflex and dorsal root reflex are mechanisms underlying the neurogenic inflammatory process. In addition, both the central nervous system and autonomic nervous system have been implicated in the development of neurogenic inflammation. However, the results in the present investigation suggest otherwise. In the absence of central and autonomic descending influences, spinal reflex loops and antidromic conduction from adjacent terminal nerve branches, the resultant capsaicin-induced neurogenic inflammatory reaction was equivalent to that produced in the presence of functional nerve conduction mechanisms. Therefore, these results lead to the hypothesis that inflammatory mediators can be directly released from afferent nerve terminals without the conduction of nerve impulses.

Unfortunately, the body of evidence supporting the above potential mechanism in the development of neurogenic inflammation is limited, and the findings from previous studies have been inconsistent. Earlier studies by Jancso et al demonstrated that axonal conduction was not necessary for the capsaicin-induced plasma extravasation and edema development since prior local anesthetic treatment did not abolish the reaction. Similarly, Szolcsanyi et al demonstrated the release of sensory neuropeptides such as substance P from the peripheral endings of sensory nerves innervating the rat trachea in the presence of local anesthesia, suggesting a direct mechanism for peptide release not mediated by an axon reflex or central descending influences. Recently, under a comparable protocol as the present study, Wong et al revealed the ineffectiveness of local anesthetic pre-treatment of the TMJ region on mustard oil-induced neurogenic inflammation. Thus, it was concluded that the direct release of inflammatory mediators from neuronal terminals is the potential mechanism underlying the neurogenic component of inflammation in the TMJ. Going without your pills? Buy cheap flomax online

Contrary to the above findings, Lundberg and Saria demonstrated the effectiveness of lidocaine in preventing neurogenic PE in the airway mucosa. Likewise, Dux et al demonstrated the inhibition of mustard oil-induced neurogenic inflammation with the pretreatment of the skin with local anesthetic. Therefore, in contrast to the findings in this present investigation, axonal conduction blockade inhibited PE in a dose-dependent manner, thus suggesting that functional nerve conduction is necessary for the development of neurogenic inflammation. Nonetheless, the discrepancies on the theory of direct release of inflammatory mediators between various investigations may be due to tissue specificities and species differences.

Alternatively, the assumption that capsaicin may induce inflammation predominantly in a nonneurogenic fashion is paradoxical since this substance is known as an important pharmacological tool used to distinguish a subset of nociceptive sensory neurons. However, since this agent is an inflammatory irritant, it is conceivable that a general inflammatory response may be evoked by the innate immune defense system due to its recognition of capsaicin as a foreign substance. Therefore, along with neuropeptides released from neuronal terminals, nonneurogenic inflammatory factors may be released by capsaicin. For example, an in vitro investigation has localized VR1 receptors on mast cells. In the event that mast cells may degranulate with the binding of capsaicin to its VR1 receptors, there is the possibility that the release of histamine may mediate inflammation by its direct action on the vasculature. Furthermore, there is a possibility that the afferents innervating the TMJ region cannot elicit neurogenic inflammation, since one study has suggested that there may be some tissue-specific trophic influences on the development of neurogenic inflammation. Therefore, a capsaicin-induced inflammatory response may be activated regardless of functional nerve conduction. Get the medication you need. Buy cialis professional online

In summary, the pretreatment of the rat TMJ region with local anesthetic failed to inhibit capsaicin-induced tissue expansion. Thus, the edema developed independent of axonal conduction, suggesting the direct release of inflammatory mediators from primary afferent nerve terminals. Hence, contrary to traditional belief, this hypothesis leads to the assumption that central and autonomic descending influences, spinal reflex loops along with antidromic stimulation from adjacent nerve terminals, are not necessary for the development of neurogenic inflammation in the rat TMJ region. Alternatively, capsaicin may act in a nonneurogenic manner; however, the mechanism by which this irritant acts remains debatable. Therefore, to fully comprehend the complex inflammatory response in the TMJ region, further investigations such as the effect of depletion of mediators on TMJ inflammation are warranted.


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