Literature DB >> 20538089

Pre-treatment with capsaicin in a rat osteoarthritis model reduces the symptoms of pain and bone damage induced by monosodium iodoacetate.

Karel-Martijn Kalff1, Mohammed El Mouedden, Jan van Egmond, Jan Veening, Leo Joosten, Gert Jan Scheffer, Theo Meert, Kris Vissers.   

Abstract

A rat model of osteoarthritis was used to investigate the effect of pre-treatment with capsaicin on the symptoms of osteoarthritis induced by the injection of monosodium iodoacetate. This model mimics both histopathology and symptoms associated of human osteoarthritis. Injection of monosodium iodoacetate, an inhibitor of glycolysis, into the femorotibial joints of rodents promotes loss of articular trabecular bone and invokes pain symptoms similar to those noted in human osteoarthritis. Twenty rats were divided in two groups either receiving placebo or monosodium iodoacetate. Each group was subdivided in two groups either receiving pre-treatment with capsaicin two weeks before monosodium iodoacetate injection or not, resulting in four groups of five rats each. The impact of a single intra-articular administration of capsaicin (0.5%) on the generation of evoked mechanical pain (hind limb weight bearing, automated von Frey monofilament and RotaRod tests) and bone lesions (micro-CT scan radiographic analyses of bone structure) following monosodium iodoacetate-induced osteoarthritis in rats was determined. Evoked mechanical pain as monitored over a period of 4 weeks after monosodium iodoacetate injection was abolished in capsaicin pre-treated animals and pain values are comparable to those of capsaicin controls. Chronic joint pathological changes such as bone erosion and trabecular damage were significantly reduced by pre-treatment with a single administration of capsaicin. Decrease of bone volume was considerably ameliorated and trabecular connectivity was substantially better in capsaicin pre-treated animals. Capsaicin, an agonist activator of the vanilloid nociceptors (TRPV1), appears to be effective in protecting bone from arthritic damage. The present results support the hypothesis that capsaicin-sensitive sensory neurons contribute to bone lesions in the monosodium iodoacetate-induced osteoarthritis rat model. Copyright (c) 2010. Published by Elsevier B.V.

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Year:  2010        PMID: 20538089     DOI: 10.1016/j.ejphar.2010.05.022

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN: 0014-2999            Impact factor:   4.432


  26 in total

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5.  Synovial macrophage-derived IL-1β regulates the calcitonin receptor in osteoarthritic mice.

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Review 6.  Osteoarthritis pain mechanisms: basic studies in animal models.

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9.  Pain, motor and gait assessment of murine osteoarthritis in a cruciate ligament transection model.

Authors:  M Z C Ruan; R M Patel; B C Dawson; M-M Jiang; B H L Lee
Journal:  Osteoarthritis Cartilage       Date:  2013-09       Impact factor: 6.576

10.  An update on targets for treating osteoarthritis pain: NGF and TRPV1.

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Journal:  Curr Treatm Opt Rheumatol       Date:  2020-05-06
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