Abstract
BackgroundThe mechanism for hip pain has been unclear because of a lack of experimental animal models. We aimed to establish an intra-articular injection technique to the rat hip and to document the effect of intra-articular mono-iodoacetate (MIA) injection to the rat hip with radiography and histology.MethodsUsing 60 6-week-old male Sprague Dawley rats, 25 μl of sterile saline (control group; n = 30) and 25 μl of sterile saline with 2 mg of MIA (MIA group; n = 30) was injected into the right hip joints via posterior approach using a 27G needle. The animals were examined with X-ray and histology 7, 14, 28, 42, and 56 days later (MIA group [n = 6] and control group [n = 6], respectively).ResultsThe MIA group showed progressive radiographic changes to the hip joint during the experimental period, whereas the control group maintained a normal appearance. The microanatomic appearance was consistent with X-ray images of progressive destruction in the MIA group and normal tissue in the control group. Osteoarthritic (OA) changes became apparent at 42 and 56 days in the MIA group.ConclusionsWe established an intra-articular injection technique to the rat hip, creating a hip OA model in the rat by intra-articular injection of MIA.
Highlights
The mechanism for hip pain has been unclear because of a lack of experimental animal models
Intra-articular injection technique to rat hip To confirm the validity of intra-articular injection into the hip, three male Sprague-Dawley (SD) rats weighing 200– 300 g at 6 weeks of age were prepared (CLEA, Tokyo, Japan)
The incidence of osteophytes was three of six hips (50 %) in the MIA group and none in the control group. This is the first study of a rat hip OA model induced by intra-articular injection of MIA
Summary
The mechanism for hip pain has been unclear because of a lack of experimental animal models. We aimed to establish an intra-articular injection technique to the rat hip and to document the effect of intra-articular mono-iodoacetate (MIA) injection to the rat hip with radiography and histology. Clinical signs of hip OA are groin pain, restricted range of motion, and gait disturbance [2, 3], which deteriorates the quality of life. It is essential to understand how histologic changes correlate with the onset of pain and joint destruction. Increases of mechanical stress and biochemical factors in the affected joints are thought to be responsible for the pathogenesis of OA. It has been suggested that tumor necrosis factor α, interleukin-6, and calcitonin generelated peptide are up-regulated in OA [6, 7]
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