Osteoarthritis is a chronic disease characterized by irreversible damage to joint structures, including loss of articular cartilage, inflammation of the synovial membrane, and alterations in the subchondral bone. Symptomatic slow-acting drugs for osteoarthritis have been proposed as treatment because of their excellent safety profile. This review summarizes some data relating to the mechanisms of action of chondroitin sulfate in the pathophysiology of osteoarthritic joint tissues.
Peer-reviewed articles obtained using pre-defined search criteria and published in the PubMed database are summarized. In addition, a relevant in press paper is included.
Chondroitin sulfate belongs to the group of glycosaminoglycans and is a major component of articular cartilage. The effect of chondroitin sulfate in patients with osteoarthritis is possibly the result of the stimulation of the synthesis of proteoglycans and the decrease in catabolic activity of chondrocytes by inhibiting the synthesis of proteolytic enzymes and other factors that contribute to cartilage matrix damage and cause the death of these cells. Chondroitin sulfate was also shown to exert anti-inflammatory activity. In addition, it acts on osteoarthritic subchondral bone osteoblasts by modulating the osteoprotegerin/receptor activator of NF-kappaB ligand ratio in favor of reduced bone resorption. It is noteworthy to mention that a head-to-head comparison of the effects of chondroitin sulfate of different origins and levels of purity on human osteoarthritic cartilage revealed the existence of a disparity in effects.
The positive effects of chondroitin sulfate on the pathophysiology of osteoarthritis are possibly due to its contribution to a proper balance between anabolism/catabolism in the articular tissues.