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Osteoclast-Mediated Pain in Osteoporosis

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Book cover Osteoporosis in Orthopedics

Abstract

Recent studies have indicated that osteoporosis patients experience idiopathic skeletal pain independent of those fractures or deformity; additionally, bisphosphonate, an effective drug for postmenopausal osteoporosis treatment, improves that skeletal pain. However, the etiology of this pain is still unknown. In this chapter, we demonstrate several data in the basis with our experiments using ovariectomized mouse model and speculate the mechanism of osteoclast-mediated pain in osteoporosis.

We have shown that pathological changes leading to increased bone resorption by osteoclast activation were related to the induction of pain-like behavior in OVX mice. This pain-like behavior was improved by the treatment with bisphosphonate. In addition, the antagonists of transient receptor potential vanilloid type 1 (TRPV1) and antagonist of acid-sensing ion channel (ASIC) 3 which are acid-sensing nociceptors and an inhibitor of vacuolar H+-ATPase known as an proton pump improved the threshold value of pain-like behaviors accompanying an improvement in the acidic environment in the bone tissue based through osteoclast inactivation. Moreover, the antagonist to P2X2/3 receptor as an ATP ligand nociceptor improved the pain-like behavior in OVX mice. These results indicated that the skeletal pain accompanying osteoporosis is possibly associated with the acidic microenvironment caused by osteoclast activation, and P2X2/3 might have a role in osteoporosis patients under a high bone turnover state.

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Correspondence to Kousuke Iba .

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Iba, K., Yamashita, T. (2016). Osteoclast-Mediated Pain in Osteoporosis. In: Shimada, Y., Miyakoshi, N. (eds) Osteoporosis in Orthopedics. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55778-4_2

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  • DOI: https://doi.org/10.1007/978-4-431-55778-4_2

  • Publisher Name: Springer, Tokyo

  • Print ISBN: 978-4-431-55777-7

  • Online ISBN: 978-4-431-55778-4

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