• International Journal of Oral Biology
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• v.38 no.4
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• pp.135-140
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• 2013

The present study investigated the effects of QX-314 on inflammatory pain of the temporomandibular joint (TMJ). Experiments were carried out on male Sprague-Dawley rats weighing 220-280 g. Under anesthesia, the TMJ of each animal was injected with $50{\mu}L$ of formalin (5%). The number of noxious behavioral responses, including rubbing or scratching of the facial region including the TMJ area, was recorded over 9 sequential 5 min intervals for each animal. Although 2.5% QX-314 did not affect formalin-induced nociceptive behavior, administration of 5% QX-314 with formalin significantly decreased the number of scratches produced by the formalin injection. Co-administration of capsaicin, a TRPV1 agonist, with 2.5% QX-314 produced significant anti-nociceptive effects whereas 2.5% QX-314 alone did not. However, the co-administration of capsaicin did not enhance the anti-nociceptive effects in the 5% QX-314-treated rats. Moreover, the co-administration of capsazepine, a TRPV1 antagonist, did not attenuate anti-nociceptive effects in the 5% QX-314-treated rats. These findings suggest that TRPV1 is effective in the transport of low but not high doses of QX-314. Moreover, a high dose of QX-314, which is not mediated by peripheral TRPV1 activity, may be viable therapeutic strategy for inflammatory pain in the TMJ.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.2
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• pp.88-98
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• 2017

To prevent toxicity from both robax platinum (methocarbamol, ibuprofen) and robaxacet (methocarbomol, acetaminophen), separately, we used stretches and naproxen as a non-steroidal anti-inflammatory drug (NSAID) to compare each effectiveness. This study used the United States Forces Korea Prescription form (Annex A-Over-The-Counter Prescription) and Alice Rich's Pain scale with robax platinum, robaxacet including narproxen. The IBM SPSS statics version 24 was used to calculate the data. The combined methocarbamol 500 mg, acetaminophen 325 mg tablet, and ibuprofen 200 mg (or naproxen) tablet can work as well as the combined methocarbamol 500 mg tablet with acetaminophen 325 mg tablet with stretches. Both methods were successful in managing pain. The drug combination of methocarbamol 500 mg, acetaminophen 325 mg and ibuprofen 200 mg tablets yielded similar benefits as the methocarbamol 500 mg and acetaminophen 325 mg tablets paired with physical stretching exercises regarding managing overall pain.

• Journal of dental hygiene science
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• v.14 no.2
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• pp.240-247
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• 2014

Acaiberry (Euterpe oleracea Mart.) is widely diffused in amazon and is known that has high antioxidant capacity and potential anti-inflammatory activities. The aim of this study was to evaluate analgesic effects of acaiberry in formalin-induced orofacial pain through p38 mitogen-activated protein kinases (p38 MAPK) and nicotinamide adenine dinucleotide phosphate 4 (NOX4) pathway. Rats were divided into 5 groups (n=6); formalin (5%, $50{\mu}L$), formalin after saline (vehicle) or acaiberry (16, 80, 160 mg/kg, intraperitoneally). The nociceptive response was investigated all of groups, p38 MAPK or NOX4 were analysed at dose of 80 mg/kg of acaiberry in rat's medulla oblongata and adrenal gland. Results indicated that acai berry produced analgesic effect in a dose-dependent manner and significantly reduced formalin-induced nociceptive response at 15~40 min. Acaiberry (80 mg/kg) decreased the increased p38 MAPK activation and NOX4 expression in medulla oblongata and adrenal gland. Based on these results, acaiberry is believed to be useful for modulation of orofacial pain and its treatments because of its anti-inflammatory and antioxidative effects.

• Journal of The Korean Dental Society of Anesthesiology
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• v.14 no.3
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• pp.157-165
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• 2014

Background: Incisional site of surgical operation become transient ischemic state and then occur reoxygenation due to vasodilatation by inflammatory reaction, the productive reactive oxygen species (ROS) give rise to many physiologic results. Apoptosis have major role on elimination of inflammatory cell and formation of granulation tissue in normal wound healing process. Remifentanil can prevent the inflammatory response and can suppress inducible nitric oxide synthase expression in a septic mouse model. After cardiopulmonary bypass for coronary artery surgery, remifentanil can also inhibit the release of biomarkers of myocardial damage. Here we investigated whether remifentanil pretreatment has cellular protective effect against hypoxia-reoxygenation in HaCaT human keratinocytes, if so, the role of apoptosis and autophagy on this phenomenon. Methods: The HaCaT human keratinocytes were exposed to various concentrations of remifentanil (0.01, 0.05, 0.1, 0.5 and 1 ng/ml) for 2 h before hypoxia (RPC/HR group). These cells were cultured under 1% oxygen tension for 24h at $37^{\circ}C$. After hypoxia, to simulate reoxygenation and recovery, the cells were reoxygenated for 12 h at $37^{\circ}C$. 3-MA/RPC/HR group was treated 3-methyladenine (3-MA), autophagy inhibitor for 1h before remifentanil treatment. Cell viability was measured using a quantitative colorimetric assay with thiazolyl blue tetrazoliumbromide (MTT, amresco), showing the mitochondrial activity of living cells. To investigate whether the occurrence of autophagy and apoptosis, we used fluorescence microscopy and Western blot analysis. Results: The viability against hypoxia-reoxygenation injury in remifentanil preconditioning keratinocytes were increased, and these cells were showed stimulated expression of autophagy 3-MA suppressed the induction of autophagy effectively and the protective effects on apoptosis. Atg5, Beclin-1, LC3-II and p62 were elevated in RPC/HR group. But they were decreased when autophagy was suppressed by 3-MA. Conclusions: Remifentanil preconditioning showed the protective effect in human keratinocytes, and we concluded that autophagy may take the major role in the recovery of wound from hypoxia-reoxygenation injury. We suggest that further research is needed about the cell protective effects of autophagy.

• Journal of the Korean Orthopaedic Association
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• v.56 no.4
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• pp.283-293
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• 2021

Degenerative disc disease has traditionally been thought of as low back pain caused by changes in the nucleus pulposus and annulus fibrous, in recent studies, however, changes in the upper and lower endplates cause degeneration of the disc, resulting in mechanical pressure, inflammatory reactions and low back pain. Recently, the bone marrow of the vertebral body-endplate-nucleus pulposus and annulus fibrous were considered as a single unit, and the relationship was explained. Once the endplate is damaged, it eventually aggravates the degeneration of the bone marrow, nucleus pulposus, and annulus fibrosus. In this process, the compression force of the annulus fibrosus increases, and an inflammatory reaction occurs due to inflammatory mediators. Hence, the sinuvertebral nerves and the basivertebral nerves are stimulated to cause back pain. If these changes become chronic, degenerative changes such as Modic changes occur in the bone marrow in the vertebrae. Finally, in the case of degenerative intervertebral disc disease, the bone marrow of the vertebral body-endplate-nucleus pulposus and annulus fibrous need to be considered as a single unit. Therefore, when treating patients with chronic low back pain, it is necessary to consider the changes in the nucleus pulposus and annulus fibrosus and a lesion of the endplate.

• The Korean Journal of Pain
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• v.26 no.4
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• pp.336-346
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• 2013

Intrathecal drug delivery is an effective and safe option for the treatment of chronic pathology refractory to conventional pain therapies. Typical intrathecal administered drugs are opioids, baclofen, local anesthetics and adjuvant medications. Although knowledge about mechanisms of action of intrathecal drugs are every day more clear many doubt remain respect the correct location of intrathecal catheter in order to achieve the best therapeutic result. We analyze the factors that can affect drug distribution within the cerebrospinal fluid. Three categories of variables were identified: drug features, cerebrospinal fluid (CSF) dynamics and patients features. First category includes physicochemical properties and pharmacological features of intrathecal administered drugs with special attention to drug lipophilicity. In the second category, the variables in CSF flow, are considered that can modify the drug distribution within the CSF with special attention to the new theories of liquoral circulation. Last category try to explain inter-individual difference in baclofen response with difference that are specific for each patients such as the anatomical area to treat, patient posture or reaction to inflammatory stimulus. We conclude that a comprehensive evaluation of the patients, including imaging techniques to study the anatomy and physiology of intrathecal environment and CSF dynamics, could become essential in the future to the purpose of optimize the clinical outcome of intrathecal therapy.

• The Korean Journal of Pain
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• v.24 no.4
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• pp.205-215
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• 2011

Background: Interventional pain management (IPM) is a branch of medical science that deals with management of painful medical conditions using specially equipped X-ray machines and anatomical landmarks. Interventional physiatry is a branch of physical medicine and rehabilitation that treats painful conditions through intervention in peripheral joints, the spine, and soft tissues. Methods: A cross-sectional study was conducted using three years of hospital records (2006 to 2008) from the Physical Medicine and Rehabilitation Department at Chittagong Medical College Hospital in Bangladesh, with a view toward highlighting current interventional pain practice in a tertiary medical college hospital. Result: The maximum amount of intervention was done in degenerative peripheral joint disorders (600, 46.0%), followed by inflammatory joint diseases (300, 23.0%), soft tissue rheumatism (300, 23.0%), and radicular or referred lower back conditions (100, 8.0%). Of the peripheral joints, the knee was the most common site of intervention. Motor stimulation-guided intralesional injection of methylprednisolone into the piriformis muscle was given in 10 cases of piriformis syndrome refractory to both oral medications and therapeutic exercises. Soft tissue rheumatism of unknown etiology was most common in the form of adhesive capsulitis (90, 64.3%), and is discussed separately. Epidural steroid injection was practiced for various causes of lumbar radiculopathy, with the exception of infective discitis. Conclusion: All procedures were performed using anatomical landmarks, as there were no facilities for the C-arm/diagnostic ultrasound required for accurate and safe intervention. A dedicated IPM setup should be a requirement in all PMR departments, to provide better pain management and to reduce the burden on other specialties.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.259-265
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• 2017

This study aimed to investigate the analgesic effect of substance P (SP) in an animal model of neuropathic pain. An experimental model of neuropathic pain, the chronic constriction injury (CCI) model, was established using ICR mice. An intravenous (i.v.) injection of SP (1 nmole/kg) was administered to the mice to examine the analgesic effects of systemic SP on neuropathic pain. Behavioral testing and immunostaining was performed following treatment of the CCI model with SP. SP attenuated mechanical allodynia in a time-dependent manner, beginning at 1 h following administration, peaking at 1 day post-injection, and decaying by 3 days post-injection. The second injection of SP also increased the threshold of mechanical allodynia, with the effects peaking on day 1 and decaying by day 3. A reduction in phospho-ERK and glial fibrillary acidic protein (GFAP) accompanied the attenuation of mechanical allodynia. We have shown for the first time that i.v. administration of substance P attenuated mechanical allodynia in the maintenance phase of neuropathic pain using von Frey's test, and simultaneously reduced levels of phospho-ERK and GFAP, which are representative biochemical markers of neuropathic pain. Importantly, glial cells in the dorsal horn of the spinal cord (L4-L5) of SP-treated CCI mice, expressed the anti-inflammatory cytokine, IL-10, which was not seen in vehicle saline-treated mice. Thus, i.v. administration of substance P may be beneficial for improving the treatment of patients with neuropathic pain, since it decreases the activity of nociceptive factors and increases the expression of anti-nociceptive factors.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.77-86
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• 2005

In this study, we examined the morphine-induced modulation of the nociceptive spinal dorsal horn neuronal activities before and after formalin-induced inflammatory pain. Intradermal injection of formalin induced time-dependent changes in the spontaneous activity of nociceptive dorsal horn neurons. In naive cats before the injection of formalin, iontophoretically applied morphine attenuated the naturally and electrically evoked neuronal responses of dorsal horn neurons. However, neuronal responses after the formalin-induced inflammation were significantly increased by morphine. Bicuculline, $GABA_A$ antagonist, increased the naturally and electrically evoked neuronal responses of dorsal horn neurons. This increase in neuronal responses due to bicuculline after the formalin-induced inflammation was larger than that in the naive state, suggesting that basal $GABA_A$ tone increased after the formalin injection. Muscimol, $GABA_A$ agonist, reduced the neuronal responses before the treatment with formalin, but not after formalin treatment, again indicating an increase in the GABAergic basal tone after the formalin injection which saturated the neuronal responses to GABA agonist. Morphine-induced increase in the spinal nociceptive responses after formalin treatment was inhibited by co-application of muscimol. These data suggest that formalin-induced inflammation increases $GABA_A$ basal tone and the inhibition of this augmented $GABA_A$ basal tone by morphine results in a paradoxical morphineinduced increase in the spinal nociceptive neuronal responses after the formalin-induced inflammation.

• Journal of Korean Neurosurgical Society
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• v.55 no.6
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• pp.370-374
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• 2014

To present a case of cauda equina syndrome (CES) caused by chronic inflammatory demyelinating polyneuropathy (CIDP) which seemed clinically similar to Charcot-Marie-Tooth disease type1 (CMT1). CIDP is an immune-mediated polyneuropathy, either progressive or relapsing-remitting. It is a non-hereditary disorder characterized by symmetrical motor and sensory deficits. Rarely, spinal nerve roots can be involved, leading to CES by hypertrophic cauda equina. A 34-year-old man presented with low back pain, radicular pain, bilateral lower-extremity weakness, urinary incontinence, and constipation. He had had musculoskeletal deformities, such as hammertoes and pes cavus, since age 10. Lumbar spine magnetic resonance imaging showed diffuse thickening of the cauda equina. Electrophysiological testing showed increased distal latency, conduction blocks, temporal dispersion, and severe nerve conduction velocity slowing (3 m/s). We were not able to find genetic mutations at the PMP 22, MPZ, PRX, and EGR2 genes. The pathologic findings of the sural nerve biopsy revealed thinly myelinated nerve fibers with Schwann cells proliferation. We performed a decompressive laminectomy, intravenous IgG (IV-IgG) and oral steroid. At 1 week after surgery, most of his symptoms showed marked improvements except foot deformities. There was no relapse or aggravation of disease for 3 years. We diagnosed the case as an early-onset CIDP with cauda equine syndrome, whose initial clinical findings were similar to those of CMT1, and successfully managed with decompressive laminectomy, IV-IgG and oral steroid.