Journal of Pain Research · 2017 · 23 citations · 35 references
MedicineOrthopaedic SurgeryOrthopedic SurgeryOrthopedicsPain MedicinePain ScienceCartilage BreakdownCartilage InjuriesJoint DiseaseJoint SurgeryOsteoarthritisPain MechanismsAnterior Cruciate Ligament InstabilityKnee MeniscectomyMechanical HyperalgesiaMusculoskeletal Pain After InjuryPain After Orthopedic SurgeryPost-traumatic Knee OsteoarthritisTrauma Pain Pathways
BACKGROUND: Osteoarthritis (OA) is a degenerative joint disease characterized by progressive cartilage degeneration, subchondral bone changes, osteophyte formation, and synovitis. A major symptom is pain that is triggered by peripheral and central changes within the pain pathways. Some surgery-induced joint instability rat models of OA were described to mimic traumatic OA. Several behavioral tests were developed to access OA-induced pain. However, follow-up in most studies usually only occurred for about 4 weeks. Since traumatic OA is a chronic disease which gradually develops after trauma, the pattern of pain might differ between early and late stages after the trauma. PURPOSE: To observe the time-dependent development of hypersensitivity after traumatic OA and to determine the best timing and methods to investigate traumatic OA-induced pain. METHODS: Anterior cruciate ligament transection plus medial meniscectomy was used to induce traumatic OA in Sprague-Dawley rats. Traumatic OA-induced pain was evaluated using four different behavioral tests for 15 weeks. RESULTS: A significant difference in mechanical hypersensitivity developed throughout the observational period. It was worst in the first 3 weeks after the operation, then became less significant after 5 weeks but persisted. There were no differences in thermal hyperalgesia or motor coordination. CONCLUSION: Traumatic OA induced mechanical hyperalgesia but did not cause thermal hyperalgesia or influence motor coordination. Furthermore, to investigate chronic pain induced by OA, the observational period should be at least 5 weeks after the intervention. These findings may help in further research and improve our understanding of traumatic OA-induced pain mechanisms.
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