作者: Joshua Allen , Ian Imbert , Joshua Havelin , Terry Henderson , Glenn Stevenson
DOI: 10.1002/ART.40101
关键词:
摘要: Objective Exercise is commonly recommended for patients with osteoarthritis (OA) pain. However, whether exercise beneficial in ameliorating ongoing pain that persistent, resistant to nonsteroidal antiinflammatory drugs (NSAIDs), and associated advanced OA unknown. Methods Rats treated intraarticular (IA) monosodium iodoacetate (MIA) or saline underwent treadmill remained sedentary starting 10 days postinjection. Tactile sensory thresholds weight bearing were assessed, followed by radiography at weekly intervals. After 4 weeks of exercise, was assessed using conditioned place preference (CPP) IA rostral ventromedial medulla (RVM)–administered lidocaine. The possible role endogenous opioids exercise-induced relief examined systemic administration naloxone. Knee joints collected micro–computed tomography (micro-CT) analysis examine pathologic changes subchondral bone metaphysis the tibia. Results Treadmill reversed MIA-induced tactile hypersensitivity asymmetry. Both RVM lidocaine D35, administered post-MIA, induced CPP but not exercised MIA-treated rats, indicating blocks Naloxone reestablished asymmetry rats undergoing aversion, dependent on opioids. Exercise did alter radiographic evidence OA. micro-CT indicated block lateral loss trabecular metaphysis, medial loss. Conclusion These findings support conclusion induces advanced, NSAID-resistant OA, likely through increased opioid signaling. In addition, blocked this model, a potential bone-stabilizing effect joint.