Osteoarthritis (OA) is a progressive degradation of articular cartilage that is a common cause of lameness for athletic horses. Oral supplementation of compounds that prevent cartilage degradation or joint injury is an attractive solution for lameness.
Glucosamine is a potential antiarthritic compound currently being marketed. It is a naturally occurring, nontoxic molecule that decreased pain and improved mobility in osteoarthritic joints in a number of human studies. In vitro (in the lab) data suggest that glucosamine may increase the synthetic activity of chondrocytes, or cartilage-producing cells. However, the biochemical basis to support its potential as an antiarthritic agent is not well documented.
One molecule thought to accelerate the progression of OA is nitric oxide. Equine chondrocytes have recently been shown to produce nitric oxide in response to two arthritogenic molecules. In addition, increased concentrations of nitric oxide and interleukin-1 are observed in synovial fluid from diseased joints. In vitro data suggest that nitric oxide activates cartilage-degrading enzymes, specifically metalloproteinases.
Articular cartilage was obtained from the carpal joint of horses (two to eight years old) euthanized for reasons other than joint problems. Researchers removed cartilage discs from the surface of the knee and placed them in a well with glucosamine or other mediums, including controls.
Nitric oxide released into media peaked the first day and returned to baseline concentrations by the third day. In three separate experiments, the addition of glucosamine prevented the increase in nitric oxide production seen in untreated wells. Additionally, a smaller dose of glucosamine partially inhibited nitric oxide production.
Results suggest that glucosamine could prevent cartilage degradation by inhibiting nitric oxide production. Future experiments will focus on how glucosamine inhibits nitric oxide and whether these results are replicated in in vivo (in the horse) experiments.
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