Surgically induced osteoarthritis in the rat results in the development of both osteoarthritis-like joint pain and secondary hyperalgesia

医学 痛觉过敏 加巴喷丁 骨关节炎 麻醉 痛觉超敏 神经病理性疼痛 内侧副韧带 罗非昔布 伤害 韧带 外科 环氧合酶 内科学 病理 化学 受体 生物化学 替代医学
作者
Susan E. Bove,Keith D. Laemont,Rachel M. Brooker,Mairead Osborn,Brian Sanchez,Roberto E. Guzman,Kenneth E. Hook,Paul Juneau,Jane R. Connor,Kenneth S. Kilgore
出处
期刊:Osteoarthritis and Cartilage [Elsevier]
卷期号:14 (10): 1041-1048 被引量:128
标识
DOI:10.1016/j.joca.2006.05.001
摘要

Summary

Objective

In the present study, we sought to develop/characterize the pain profile of a rat model of surgically induced osteoarthritis (OA).

Methods

OA was surgically induced in male Lewis rats (200–225g) by transection of the medial collateral ligament and medial meniscus of the femoro-tibial joint. In order to characterize the pain profile, animals were assessed for a change in hind paw weight distribution (HPWD), development of mechanical allodynia, and the presence of thermal and mechanical hyperalgesia. Rofecoxib and gabapentin were examined for their ability to decrease change in weight distribution and tactile allodynia.

Results

Transection of the medial collateral ligament and medial meniscus of male Lewis rats resulted in rapid (<3 days) changes in hind paw weight bearing and the development of tactile allodynia (secondary hyperalgesia). There was, however, no appreciable effect on thermal hyperalgesia or mechanical hyperalgesia. Treatment with a single dose of rofecoxib (10mg/kg, PO, day 21 post surgery) or gabapentin (100mg/kg, PO, day 21 post surgery) significantly attenuated the change in HPWD, however, only gabapentin significantly decreased tactile allodynia.

Conclusion

The rat medial meniscal tear (MMT) model mimics both nociceptive and neuropathic OA pain and is responsive to both a selective cylooxygenase-2 (COX-2) inhibitor commonly utilized for OA pain (rofecoxib) and a widely prescribed drug for neuropathic pain (gabapentin). The rat MMT model may therefore represent a predictive tool for the development of pharmacologic interventions for the treatment of the symptoms associated with OA.
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