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

Ito, Akitoshi; Yoshimura, Michihiro

doi:10.1177/1744806917720316

Cited by 22 publications

(16 citation statements)

References 101 publications

(159 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Ovariectomized rats with hyperalgesia improved after subcutaneous calcitonin administration (20 U/kg/day) for 3 weeks in a postmenopausal osteoporosis and chronic pain model 27. Although calcitonin disappears within 2 hours of injection into human and rat plasma, subsequent injection of calcitonin gradually enhances antihyperalgesic effects 28. These effects are maintained for several days after cessation of calcitonin administration 21,26.…”

Section: Discussionmentioning

confidence: 99%

Analgesic effects of calcitonin on radicular pain in male rats

Terashima¹,

Takebayashi²,

Jimbo³

et al. 2019

JPR

View full text Add to dashboard Cite

PurposeRadicular pain is a frequently observed symptom of lumbar disk herniation or lumbar spinal canal stenosis. Achieving radicular pain relief is difficult. This type of pain may progress to chronic neuropathic pain. Calcitonin (elcatonin [eCT]) has been used mainly for hypercalcemia and pain associated with osteoporosis. The purpose of this study was to investigate analgesic effects of repeated eCT administration on radicular pain in male rats and changes in mRNA-expression levels of voltage-dependent sodium channels in the dorsal root ganglion (DRG).MethodsSeventy male Sprague-Dawley rats were used. A right L5 hemilaminectomy and an L5–L6 partial facetectomy were performed to expose the right L5 nerve root. Under a microscope, the right L5 spinal nerve root was tightly ligated extradurally with 8-0 nylon suture proximally to the DRG to cause radicular pain in rats. Mechanical hyperalgesia, thermal hyperalgesia, and analgesic effects of eCT were compared among rats with radicular pain that received eCT, those that received the vehicle, and sham rats that received the vehicle. Real-time reverse-transcription PCR was performed to measure mRNA-expression levels of tetrodotoxin-sensitive (NaV1.3 and NaV1.6) and tetrodotoxin-resistant (NaV1.8 and NaV1.9) sodium channels in the DRG.ResultsMechanical and thermal hyperalgesic reactions occurring in rats with radicular pain significantly improved on days 5 and 9 of eCT administration, respectively. In rats with radicular pain, mRNA-expression levels of NaV1.3, NaV1.8, and NaV1.9 increased. After repeated eCT administration, mRNA-expression levels of these sodium channels in rats with radicular pain improved to the same levels as in sham rats.ConclusionThe present study demonstrated that repeated systemic eCT administration was effective for radicular pain. No serious side effects of eCT have been reported thus far. Therefore, calcitonin may be a preferred therapeutic option for patients with radicular pain or for those requiring long-term treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Analgesic effects of calcitonin on radicular pain in male rats

Terashima¹,

Takebayashi²,

Jimbo³

et al. 2019

JPR

View full text Add to dashboard Cite

show abstract

“…Serotonin has an analgesic effect on chronic pain in humans and animals (28). Calcitonin in ovariectomized rats can cause the release of glutamate from C-afferent fibers and can also normalize the expression of sodium channel in damaged peripheral nerves (29). Immunohistochemical studies have also shown that the PAG area that contains dopaminergic neurons is involved in the analgesic system.…”

Section: Discussionmentioning

confidence: 99%

“…Despite its analgesic effects, oral sCT does not have renewable benefits for patients suffering from knee osteoarthritis (41). Studies suggest that calcitonin can alleviate back pains of patients suffering from neuropathic pain or osteoporosis by altering the expression of channels or receptors (29,42).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Salmon Calcitonin on the Concentrations of Periaqueductal Gray Monoamines in the Formalin Test

2019

View full text Add to dashboard Cite

Background: The receptors of salmon calcitonin, located on certain areas of the brain such as the periaqueductal gray matter, are responsible for pain modulation. Aims: The effects of intracerebroventricular injection of salmon calcitonin on the behavioral response to pain and on the levels of monoamines in the periaqueductal gray were explored using a biphasic animal model of pain. Study Design: Animal experiment. Methods: A total of 45 male rats were divided into four groups (n=6). Salmon calcitonin was injected into the lateral ventricle of the brain (1.5 nmol, with a volume of 5 μL). After 20 min, 2.5% formalin was subcutaneously injected into the right leg claw, and pain behavior was recorded on a numerical basis. At the time of the formalin test, the periaqueductal gray area was microdialized. High-performance liquid chromatography method was used to gauge the levels of monoamines and their metabolites. Results: Intracerebroventricular injections of salmon calcitonin resulted in pain reduction in the formalin test (p<0.05). The dialysate concentrations of serotonin, dopamine, norepinephrine, 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic, and 4-hydroxy-3-methoxyphenylglycol increased in the periaqueductal gray area in different phases of the formalin pain test (p<0.05). Conclusion: Salmon calcitonin reduced pain by increasing the concentrations of monoamines and the metabolites derived from them in the periaqueductal gray area.

show abstract

“…41 Experiments conducted by Ito and Yoshimura on ovariectomized rats demonstrate that calcitonin may decrease neuronal hyperexcitability by restoring 5-HT receptors and normalizing voltage-dependent sodium channels anti-hyperalgesic effect. 38 Another potential explanation poses the possibility of anti-inflammatory properties of calcitonin by blocking prostaglandin E2 synthesis. 42 Experiments on guinea pig lungs perfused with arachidonic acid were treated with calcitonin resulting in a 50% decrease in arachidonic acid and thus a reduction in the prostaglandin system.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Calcitonin (FORTICAL, MIACALCIN) for the treatment of vertebral compression fractures

et al. 2021

View full text Add to dashboard Cite

Osteoporosis is a common condition affecting the musculoskeletal system. It carries with it increased risks of fracture in many areas of the body, leading to reduced quality of life, limited mobility, and other long-term implications such as chronic pain. Vertebral compression fractures are a common development in patients with osteoporosis. Current treatment options focus on reducing pain; preventative methods are somewhat limited and focus on minimizing risk factors for the development of osteoporosis. In this review, we explore the use of calcitonin (FORTICAL, MIACALCIN) to treat vertebral compression fractures (VCFs). Recent FindingsOsteoporosis had a prevalence of more than 10% in the United States in 2010. The CDC estimates that nearly 25% of women over age 65 have findings of osteoporosis, which include low spinal bone mass. The condition is highly prevalent and, in an aging U.S. population, quite clinically relevant. Risk factors for development include advanced age, cigarette smoking, medications, reduced physical activity, and low calcium and vitamin D intake. Family history may also play a role. Diagnosis is made based on bone mineral density. Standard therapy for VCFs in osteoporosis includes analgesic medications, such as NSAIDs and biphosphonates, and surgical intervention. NSAIDs address the chronic pain that is a common long-term effect of VCFs. Biphosphonates have recently been used to attempt to halt the progression and provide prevention. Surgical interventions such as balloon kyphoplasty and vertebroplasty are typically reserved for patients who have failed other methods. Calcitonin is a peptide naturally produced by the human body, released from the parathyroid gland. It binds to osteoclasts, inhibiting them from inducing bone resorption. By relatively unknown mechanisms, it also appears to cause endorphin release and mitigate pain. Clinical data has shown safety and efficacy for exogenous calcitonin in reducing bone turnover and reducing VCF-induced pain.

show abstract

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

Cited by 22 publications

References 101 publications

Analgesic effects of calcitonin on radicular pain in male rats

Analgesic effects of calcitonin on radicular pain in male rats

The Effects of Salmon Calcitonin on the Concentrations of Periaqueductal Gray Monoamines in the Formalin Test

Calcitonin (FORTICAL, MIACALCIN) for the treatment of vertebral compression fractures

Contact Info

Product

Resources

About