Anti-inflammatory drugs as well as glucosamine salts are widely used for the treatment of osteoarthrosis.  Anti-inflammatory drugs relieve pain, but they inhibit cartilage proteoglycan (PP) synthesis. A standard method which uses "in vitro" cultures of articular cartilage capsules from rat femoral heads removed from the acetabular cavity and radioactive precursors as well as analytical determinations has been chosen for these studies.  Glucosamine HCl enhances tritiated proline as well as radioactive sulfate incorporation by cartilage. Non steroidal antiinflammatory drugs (NSAD) inhibit either protein and sulfated mucopolysaccharides (SMPS) synthesis in agreement with previously reported data in favor of a common control mechanism for both synthesis.  Glucosamine reduces slightly the depression caused by NSAD, and this might be explained on the basis of consideration of the biochemical steps of UPS synthesis known to be inhibited by NSAD: glucosamine-GP-synthetase, acetyl-CoA-synthetase, and UDPG-dehydrogenase.  Only the first inhibition may be avoided by glucosamine. NSAD with depressing activity on MPS synthesis should used very carefully for osteoarthrosis  therapy, because they might exert a negative influence on the already unbalanced articular cartilage metabolism.