Abstract
Lumbar facet joint (LFJ) osteoarthritis (OA) is an important etiology of low back pain. Several animal models of LFJ OA have been established using intraarticular injection of various chemicals. This study aimed to establish a rat model of LFJ OA using urinary plasminogen activator (uPA). Sprague-Dawley rats were treated with intraarticular injection in the L5-L6 facet joints with uPA (OA group, n = 40) or normal saline (vehicle group, n = 40). Mechanical and thermal hyperalgesia in the ipsilateral hind paws were evaluated using von Frey hairs and a thermoalgesia instrument, respectively. Toluidine blue staining, hematoxylin-eosin staining, and immunohistochemical examination of the LFJ was performed. Treatment with uPA induced cartilage damage, synovitis, and proliferation of synovial cells in the fact joints. The OA group showed significantly higher hyperalgesia in the hind paws in comparison with the vehicle group and normal controls (P < 0.05). Expression of IL-1β, TNF-α, and iNOS in the LFJ cartilage in the OA group was significantly increased (P < 0.05). A rat model of LFJ OA was successfully established using intraarticular injection of uPA. This animal model is convenient and shows good resemblance to human OA pathology.
Highlights
Establishment of a rat model of lumbar facet joint osteoarthritis using intraarticular injection of urinary plasminogen activator
We tried to establish a rat model of Lumbar facet joint (LFJ) OA using intraarticular injection of urinary plasminogen activator (uPA). uPA is a serine protease and its primary physiological substrate is plasminogen
It has been found that uPA plays important roles in the degeneration of extracellular matrix in the osteoarthritic cartilage[6], and levels of uPA in the articular cartilage and synovium are associated with the severity of cartilage damage[18]
Summary
Establishment of a rat model of lumbar facet joint osteoarthritis using intraarticular injection of urinary plasminogen activator. Lumbar facet joint (LFJ) osteoarthritis (OA) is an important etiology of low back pain. Several animal models of LFJ OA have been established using intraarticular injection of various chemicals. This study aimed to establish a rat model of LFJ OA using urinary plasminogen activator (uPA). A rat model of LFJ OA was successfully established using intraarticular injection of uPA. This animal model is convenient and shows good resemblance to human OA pathology. We established a rat model of LFJ OA using intraarticular injection of uPA and evaluated the various animal behavior and pathological changes
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