The Suppressive Effect of Hyaluronan on Nitric Oxide Production and Cell Apoptosis in the Central Region of Meniscus Following Partial Meniscectomy

Osteoarthritic changes in tibial articular cartilage following total or partial meniscectomy have been reported in both human7,15 and animal studies.10,13 function.9,12 In addition to the biomechanical effects of joint destabilization, it has been suggested that increased production of catabolic biomolecular mediators such as nitric oxide(NO) contribute to the pathogenesis of articular cartilage during developing osteoarthritis.1 NO has been reported to have catabolic effects on chondrocytes including inhibition of collagen and proteoglycan synthesis 2,6 and modulation of metalloproteinase activity.11 Recently, our laboratories reported that NO was increased in the meniscus during experimentally induced osteoarthritis5 and established that NO production was limited primarily to the central region of this tissue following partial meniscectomy.8 We hypothesized that the negative effects of NO would be manifested by the impaired ability of the injured meniscus to undergo repair and remodeling resulting in increased joint pathology and symptoms of osteoarthritis. Hyaluronan (HA) is a molecule that has been used clinically in a symptomatic procedure for the treatment of osteoarthritis. In an animal study we demonstrated that HA had a chondroprotective effect on articular cartilage and enhanced meniscal regeneration and remodeling following meniscal injury.14 In light of these findings, we proposed that HA might be able to inhibit nitric oxide production and cell apoptosis in the central region of the meniscus following partial meniscectomy. In the present study we have demonstrated the ability of HA to suppress both nitric oxide production and cell apoptosis in the central region of the meniscus 6 weeks after partial meniscectomy.