Early Dexamethasone Relieves Trigeminal Neuropathic Pain

Han, Seung Ro; Yeo, Sang P.; Lee, Min K; Bae, Yong Chul; Ahn, Dongbin

doi:10.1177/0022034510374056

Cited by 45 publications

(39 citation statements)

References 23 publications

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“…Recently, Han et al reported that early treatment with dexamethasone produces a prolonged inhibition of mechanical allodynia in a rat model of trigeminal neuropathic pain produced by mal-positioned dental implants [10]. Daily treatment with dexamethasone significantly reduced the expression of p-p38 MAPK and p-NF-κB on POD 7 in our present experiments.…”

Section: Discussionsupporting

confidence: 72%

Behavioral Evidence for the Differential Regulation of p-p38 MAPK and p-NF-κB in Rats with Trigeminal Neuropathic Pain

et al. 2011

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BackgroundWe investigated the differential regulation of p-p38 MAPK or p-NF-κB in male Sprague-Dawley rats with inferior alveolar nerve injury resulting from mal-positioned dental implants. For this purpose, we characterized the temporal expression of p-p38 MAPK or p-NF-κB in the medullary dorsal horn and examined changes in nociceptive behavior after a blockade of p-p38 MAPK or p-NF-κB pathways in rats with trigeminal neuropathic pain.ResultsUnder anesthesia, the left lower second molar was extracted and replaced with a mini dental implant to intentionally injure the inferior alveolar nerve. Western and immunofluorescence analysis revealed that p-p38 MAPK is upregulated in microglia following nerve injury and that this expression peaked on postoperative day (POD) 3 through 7. However, the activation of p-NF-κB in astrocyte peaked on POD 7 through 21. The intracisternal administration of SB203580 (1 or 10 μg), a p38 MAPK inhibitor, on POD 3 but not on POD 21 markedly inhibits mechanical allodynia and the p-p38 MAPK expression. However, the intracisternal administration of SN50 (0.2 or 2 ng), an NF-κB inhibitor, on POD 21 but not on POD 3 attenuates mechanical allodynia and p-NF-κB expression. Dexamethasone (25 mg/kg) decreases not only the activation of p38 MAPK but also that of NF-κB on POD 7.ConclusionsThese results suggest that early expression of p-p38 MAPK in the microglia and late induction of p-NF-κB in astrocyte play an important role in trigeminal neuropathic pain and that a blockade of p-p38 MAPK at an early stage and p-NF-κB at a late stage might be a potential therapeutic strategy for treatment of trigeminal neuropathic pain.

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Section: Discussionsupporting

confidence: 72%

Behavioral Evidence for the Differential Regulation of p-p38 MAPK and p-NF-κB in Rats with Trigeminal Neuropathic Pain

et al. 2011

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“…In the present study, similar results were obtained with the daily treatment with Dex after CION. Our results are in agreement with Han and co-workers, which also showed that early, but not the late, treatment with Dex at much higher doses reduced the mechanical hyperalgesia induced by malpositioned dental implant (Han et al, 2010). Since it has been shown that Dex acts by blocking the synthesis of cytokines (Safieh-Garabedian et al, 1995), we evaluated if the de novo cytokine synthesis occurs only at the beginning or later after neuropathic pain induction.…”

Section: Discussionsupporting

confidence: 91%

Etanercept reduces thermal and mechanical orofacial hyperalgesia following inflammation and neuropathic injury

Coelho

Bastos-Pereira

Fraga

et al. 2014

European Journal of Pain

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“…Recently, application of a long-acting anti-inflammatory drug diprospan in treating primary TN through local nerve cord injection has achieved satisfactory effects [1][2][3][4] . However, the action mechanism of this agent and the pathophysiological changes in the trigeminal nerve remain unclear.…”

mentioning

confidence: 99%

“…However, the action mechanism of this agent and the pathophysiological changes in the trigeminal nerve remain unclear. Some studies suggested that the anti-inflammatory, anti-rheumatic, and anti-anaphylactic properties of disprospan were involved [1,2] . In this study, rat model of TN was established by inducing chronic constriction injury (CCI) to the left trigeminal nerve of the rats.…”

mentioning

confidence: 99%

Analgesic effect of diprospan in rats with trigeminal neuralgia

Wang

Cao

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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This study examined the analgesic effect of diprospan in rats with trigeminal neuralgia. Rat model of trigeminal neuralgic pain was established by loosely ligating the left infraorbital branch of the trigeminal nerve. After allodynia developed, the rats were randomly divided into 2 groups (n=20 in each): diprospan group, in which the rats received diprospan (7 mg/mL, 0.1 mL) injected to the left infraorbital foramen area; control group, in which saline (0.1 mL) was administered as the same manner as the diprospan group. The pain threshold (PT) in the left infraorbital area was measured before and 2, 6, and 8 weeks after the administration. The expression of neuropeptides [substance P, preprotachykinin A (PPTA), calcitonin gene-related peptide (CGRP)] in the trigeminal nerve was detected at the same time points as the PT measurement by immunohistochemistry or in situ hybridization method. The results showed that in the diprospan group, the PT was 10.65 ± 1.26, 10.77 ± 1.19 and 14.13 ± 1.34 g 2, 6, and 8 weeks after the administration respectively, significantly higher than that before the administration (PT value: 0.36 ± 0.11) (P<0.05 for each). In the saline group, the PT was 0.37 ± 0.13, 0.66 ± 0.09, 4.45 ± 1.29 and 13.72 ± 1.72 g before and 2, 6, and 8 weeks after the administration respectively with differences being significant between before and 6, 8 weeks after the administration (P<0.01). No significant difference existed in the PT between the diprospan group and the saline group at pre-administration (P>0.05). The PT in the diprospan group was significantly greater than that in the saline group 2 and 6 weeks post-administration (P<0.05). In the diprospan group, the expression levels of neuropeptides were significantly reduced as compared with those in the saline group 2 and 6 weeks post-administration (P<0.05). It was concluded that diprospan has an obvious analgesic effect on the trigeminal neuropathic pain partly by reducing the expression of neuropeptides in the trigeminal ganglia.

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Early Dexamethasone Relieves Trigeminal Neuropathic Pain

Cited by 45 publications

References 23 publications

Behavioral Evidence for the Differential Regulation of p-p38 MAPK and p-NF-κB in Rats with Trigeminal Neuropathic Pain

Behavioral Evidence for the Differential Regulation of p-p38 MAPK and p-NF-κB in Rats with Trigeminal Neuropathic Pain

Etanercept reduces thermal and mechanical orofacial hyperalgesia following inflammation and neuropathic injury

Analgesic effect of diprospan in rats with trigeminal neuralgia

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