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Mechanisms of the analgesic effect of calcitonin on chronic pain by alteration of receptor or channel expression.

ABSTRACT: The polypeptide hormone calcitonin is well known clinically for its ability to relieve osteoporotic back pain and neuropathic pain such as spinal canal stenosis, diabetic neuropathy, chemotherapy-induced neuropathy, and complex regional pain syndrome. Because the analgesic effects of calcitonin have a broad range, the underlying mechanisms of pain relief by calcitonin are largely unknown. However, recent studies using several types of chronic pain models combined with various methods have been gradually clarifying the mechanism. Here, we review the mechanisms of the analgesic action of calcitonin on ovariectomy-induced osteoporotic and neuropathic pain. The analgesic action of calcitonin may be mediated by restoration of serotonin receptors that control selective glutamate release from C-afferent fibers in ovariectomized rats and by normalization of sodium channel expression in damaged peripheral nerves. Serotonin receptors are reduced or eliminated by the relatively rapid reduction in estrogen during the postmenopausal period, and damaged nerves exhibit hyperexcitability due to abnormal expression of Na+ channel subtypes. In addition, in chemotherapy-induced peripheral neuropathy, inhibition of signals related to transient receptor potential ankyrin-1 and melastatin-8 is proposed to participate in the anti-allodynic action of calcitonin. Further, an unknown calcitonin-dependent signal appears to be present in peripheral nervous tissues and may be activated by nerve injury, resulting in regulation of the excitability of primary afferents by control of sodium channel transcription in dorsal root ganglion neurons. The calcitonin signal in normal conditions may be non-functional because no target is present, and ovariectomy or nerve injury may induce a target. Moreover, it has been reported that calcitonin reduces serotonin transporter but increases serotonin receptor expression in the thalamus in ovariectomized rats. These data suggest that calcitonin could alleviate lower back pain in patients with osteoporosis or neuropathic pain by the alteration in receptor or channel expression.

SUBMITTER: Ito A

PROVIDER: S-EPMC5524232 | biostudies-other | 2017 Jan-Dec

REPOSITORIES: biostudies-other

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Project description:UnlabelledOpioids are regularly administered in acute and cancer pain. In chronic non-cancer pain (CNCP), however, their use is controversial. Previous meta-analyses and randomized controlled trials (RCTs) lack methodological homogeneity and comparable data. Here we analysed the maximum analgesic efficacies of opioids and non-opioids compared with placebo, and of physiotherapy and psychotherapy compared with active or waiting-list controls. We screened 3647 citations and included RCTs if treatment duration was at least 3 weeks, data were sufficient for meta-analysis, and criteria for high quality were met. Only 46 studies (10 742 patients) met the criteria. Weighted and standardized mean differences (WMD, SMD) between pain intensities were pooled to conduct separate meta-analyses for each treatment category. At the end of treatment the WMD for pain reduction (100-point scale) was 12.0 for 'strong' opioids, 10.6 for 'weak' opioids, 8.4 for non-opioids (each vs. placebo), 5.5 for psychotherapy and 4.5 for physiotherapy (each vs. active controls). Dropout rates were high in pharmacological studies. The 95% confidence intervals using the outcomes of control groups did not indicate statistical differences between efficacies of the five interventions. Because not enough eligible head-to-head trials were available, our analysis is limited to adjusted indirect comparisons. The heterogeneity of pre-post pain differences in control groups did not allow the definition of a common comparator. In conclusion, although there were statistically significant differences between maximum treatment efficacies, no intervention per se produced clinically important improvements in average pain intensity. Thus, opioids alone are inappropriate and multimodal treatment programmes may be required for CNCP.Linked articlesThis article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2.

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Mechanisms of the analgesic effect of calcitonin on chronic pain by alteration of receptor or channel expression.

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