M Dougados1. 1. René Descartes University, Clinique de Rhumatologie, Hôpital Cochin, Paris, France. maxime.dougados@cch.ap_hop_paris.fr
Abstract
OBJECTIVES: Currently, available therapies for managing osteoarthritis (OA) provide symptomatic relief. Theoretical evidence suggests that exogenous hyaluronan (HA) administered as an intra-articular injection may slow disease progression. The purpose of this review is to discuss cellular and immunologic effects of HA that could affect OA progression and to present data from a clinical trial that evaluated HA structural effects. METHODS: The medical and scientific literature regarding the cellular, immunologic, and structural effects of HA on the joint environment and function are reviewed. RESULTS: Cellular effects of exogenous HA that affect the joint include increasing endogenous HA synthesis, stimulating proteoglycan synthesis, and inhibiting the release of chondrodegrading enzymes. The immunologic effects of HA are inhibition of mononuclear cell phagocytosis and leukocyte migration, chemotaxis, and phagocytosis. Also, HA is a free radical scavenger. In a pilot study using arthroscopy, cartilage deterioration was less in the HA-treated group compared with the control group. CONCLUSIONS: Considerable evidence supports the positive effects of HA on joint cellular and immunologic function. However, further clinical studies are needed to determine whether these effects are valuable in altering the progression of OA.
OBJECTIVES: Currently, available therapies for managing osteoarthritis (OA) provide symptomatic relief. Theoretical evidence suggests that exogenous hyaluronan (HA) administered as an intra-articular injection may slow disease progression. The purpose of this review is to discuss cellular and immunologic effects of HA that could affect OA progression and to present data from a clinical trial that evaluated HA structural effects. METHODS: The medical and scientific literature regarding the cellular, immunologic, and structural effects of HA on the joint environment and function are reviewed. RESULTS: Cellular effects of exogenous HA that affect the joint include increasing endogenous HA synthesis, stimulating proteoglycan synthesis, and inhibiting the release of chondrodegrading enzymes. The immunologic effects of HA are inhibition of mononuclear cell phagocytosis and leukocyte migration, chemotaxis, and phagocytosis. Also, HA is a free radical scavenger. In a pilot study using arthroscopy, cartilage deterioration was less in the HA-treated group compared with the control group. CONCLUSIONS: Considerable evidence supports the positive effects of HA on joint cellular and immunologic function. However, further clinical studies are needed to determine whether these effects are valuable in altering the progression of OA.