5 research outputs found
Activation of voltage-gated KCNQ/Kv7 channels by anticonvulsant retigabine attenuates mechanical allodynia of inflammatory temporomandibular joint in rats
<p>Abstract</p> <p>Background</p> <p>Temporomandibular disorders (TMDs) are characterized by persistent orofacial pain and have diverse etiologic factors that are not well understood. It is thought that central sensitization leads to neuronal hyperexcitability and contributes to hyperalgesia and spontaneous pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are currently the first choice of drug to relieve TMD pain. NSAIDS were shown to exhibit anticonvulsant properties and suppress cortical neuron activities by enhancing neuronal voltage-gated potassium KCNQ/Kv7 channels (M-current), suggesting that specific activation of M-current might be beneficial for TMD pain.</p> <p>Results</p> <p>In this study, we selected a new anticonvulsant drug retigabine that specifically activates M-current, and investigated the effect of retigabine on inflammation of the temporomandibular joint (TMJ) induced by complete Freund's adjuvant (CFA) in rats. The results show that the head withdrawal threshold for escape from mechanical stimulation applied to facial skin over the TMJ in inflamed rats was significantly lower than that in control rats. Administration of centrally acting M-channel opener retigabine (2.5 and 7.5 mg/kg) can dose-dependently raise the head withdrawal threshold of mechanical allodynia, and this analgesic effect can be reversed by the specific KCNQ channel blocker XE991 (3 mg/kg). Food intake is known to be negatively associated with TMJ inflammation. Food intake was increased significantly by the administration of retigabine (2.5 and 7.5 mg/kg), and this effect was reversed by XE991 (3 mg/kg). Furthermore, intracerebralventricular injection of retigabine further confirmed the analgesic effect of central retigabine on inflammatory TMJ.</p> <p>Conclusions</p> <p>Our findings indicate that central sensitization is involved in inflammatory TMJ pain and pharmacological intervention for controlling central hyperexcitability by activation of neuronal KCNQ/M-channels may have therapeutic potential for TMDs.</p
Similarities and differences of estrogen in the regulation of temporomandibular joint osteoarthritis and knee osteoarthritis
Background. Temporomandibular joint
osteoarthritis (TMJOA) and knee osteoarthritis (knee
OA) are two kinds of common osteoarthritis (OA) that
are characterized by chronic degeneration of soft and
hard tissues around joints. Their gender and age
differences suggest that there are similarities and
differences between the pathogenic mechanisms of
TMJOA and knee OA.
Objective. To review recent studies on the effect of
estrogen on TMJOA and knee OA, and summarize their
possible pathogenesis and molecular mechanisms.
Sources. Articles up to present reporting the
relationship of estrogen and TMJOA or knee OA are
included. An extensive electronic search was conducted
of databases including PubMed, Web of science core
collection.
Conclusion. According to epidemiological
investigations, TMJOA primarily happens to females of
puberty and childbearing age, while knee OA mainly
affects postmenopausal women. Epidemiological
investigation and experimental research suggest that
estrogen may have a different effect on TMJ and on
knee. Though estrogen regulates TMJOA and knee OA
via estrogen-related receptors (ERR), their pathogenesis
and pathway of estrogen regulation are different. To find
out the accurate regulation of estrogen on TMJOA and
knee OA, specific pathways and molecular mechanisms
still need further exploration