Glucosamine has been characterized as a non-rapid acting drug indicated for the treatment of OA. Its cartilage protecting effect has not been demonstrated in a in vivo model (in people). However, in vitro ( Laboratory work with chemicals etc...)  experimental evidence suggest it could have a favorable role in maintaining cartilage health. Examples of these beneficial roles include:

• If glucosamine is added to chondrocytes of osteoarthritic cartilage, a dose-dependent increase in proteoglycan synthesis occurs.
• In the rabbit model, there has been a suggestion that glucosamine sulfate slows the progression of cartilage lesions.
• In animal models of arthritis, glucosamine has been demonstrated to stabilize cell membranes, reduce the generation of oxygen-free radicals by macrophages, and inhibit lysosomal enzymes.
• It may inhibit interleukin-1-induced nitric oxide activity, which mediates chondrocyte cell death. Glucosamine also may inhibit interleukin-1-induced increases in aggrecanase activity, which could lead to preservation of proteoglycan.
• New studies suggest that glucosamine may suppress neutrophils and their inflammatory effect.
• In human fetal chondrocytes, glucosamine increases type II collagen production, although this effect was not seen in adult chondrocytes.

In summary,  researchers believe that glucosamine beneficially affects the imbalance between rates of synthesis and degradation of cartilage proteoglycans believed to be present in OA.  Recent evidence suggests that glucosamine not only supports the production of cartilage, but also has an anti-inflammatory effect.

OA sufferers will attest to the analgesic affects of glucosamine.  Researchers have not yet discovered the exact mechanism of this.  It is known that glucosamine does not work on the cyclooxygenase pathway as do NSAIDs.