Mechanism of action The cartilage matrix. The joint space is filled with synovial fluid.<unk> s are attached to proteins, which are attached to a strand of hyaluronic acid to create a "bottle brush". Normally, joint cartilages have proteoglycan complexes, which are proteins with side chains made of<unk> s such as keratan sulfate and chondroitin sulfate attached to strands of hyaluronic acid. The<unk>  side chains are polyanionic, which causes adjacent side chains to push each other away and create a "bottle brush", where hyaluronic acid is the stem and the side chains are the bristles. When pressure is exerted on the joint, fluids move between the chondrocytes and synovial fluid, exchanging nutrients. In degenerative joint disease, the proteoglycan complexes start disappearing, and the hyaluronate becomes poorer in quality and scarcer. This lowers the viscosity of the synovial fluid (which increases friction) and causes white blood cells and enzymes to enter and effect cartilage degradation and inflammation. Steroids that are released as a result kill the chondrocytes. The remaining chondrocytes have trouble exchanging nutrients with the synovial fluid, which would allow them to repair some damages. The mechanism of<unk>  in vivo is based on observations and studies in vitro.<unk>  inhibits many of the catabolic enzymes that degrade cartilage, proteoglycans, and hyaluronic acid. The enzymes that are inhibited include serine proteases, which play a role in the IL-1 degradation of proteoglycans and collagen; lysosomal enzymes that cause proteoglycans to dissociate from hyaluronic acid; elastase; metalloproteinases such as stromelysin, which degrade cartilage matrix proteins; collagenases such as cathepsin B1; and hyaluronidase.<unk>  inhibits the synthesis of prostaglandin E2, which is released upon joint injury and causes inflammation, increases the loss of proteoglycan, and reduces the threshold of pain receptors. Inhibiting the complement pathway further reduces inflammation, most likely by altering C-reactive protein. The inhibition of blood coagulation reduces resultant fibrinolysis, which would cause cell death and increase local inflammation.<unk>  also stimulates the synthesis of<unk> s, hyaluronic acid, and collagen, which increase synovial viscosity. It cannot, however, completely reverse the disappearance of cartilage, nor can it reverse bone loss caused by arthritis. Pharmacokinetics<unk>  reaches peak blood concentration in 20–40 minutes when injected intramuscularly; 30–40% of it binds to blood proteins. It enters all tissues, reaching cartilage within two hours. When<unk>  reaches the synovial fluid, it is then taken up by the cartilage matrices, with osteoarthritic cartilage showing a stronger preference for taking it up. It reaches its peak levels in the joints at 48 hours, and lasts up to 96 hours, before leaving and being excreted by the kidneys.
Polysulfated glycosaminoglycan
Hyaluronic acid
Pentosan polysulfate
Self-protein
Cerebroside
Tetrameric protein
Lecithin
Conjugated linoleic acid