Expression and production of spinal cyclooxygenase 1 and 2 in the model of experimental osteoarthritis
Abstract
Osteoarthritis (OA) is a degenerative joint disease.Th ejoints are characterized by a progressive degeneration of articular cartilage leading to inflammattion and pain.In attempt to study the pathophysiology of OA, numerous experimental model that mimic human OA have been developed.Chemical models of OA involve intraarticular injection of chemical compounds that can have a number of effects on joint physiology.Surgical models of OA induce joint instability by partial menisectomy.One of the most frequently used model is the model of monoiodoacetate (MIA) induced OA.Local injection of monoiodoacetate, an inhibitor of glycolysis,disrupt chondrocyte metabolism and produces cartilage degeneration.In mice,injection of monoiodoacetate led to strong inhibition of proteoglycan synthesis in the patella and in the medial part of tibial plateau.The loss of locomotor activity and the severity of cartilage lesions in patella were observed in rats injected with MIA.It was previously described, the important role of synovial cyclooxygenase-1 in patient with primary osteoarthritis.The role of spinal cyclooxygenase (COX) isoenzymes in the ostearthritis is not known.The aim of the present study was to ascertain the role of spinal COX-1 and COX-2 in the model of monoiodoacetate induced ostearthritis