The tidemark is a metabolically active zone in the calcified layer of the cartilage in which it is possible to show that there is calcifying activity even over a short period of time using a tetracycline labelling technique. The tidemark slowly advances in the direction of the non-calcified cartilage and analysis of double-tetracycline labelled cartilage shows that this is not an appositional phenomenon like that occurring in bone, but that, where present, several tidemarks can be labelled at the same time. Each tidemark may therefore be metabolically active and it is not just the tidemark adjacent to hyaline cartilage which incorporates calcium.

To test the hypothesis that non-steroidal anti-inflammatory drugs (NSAIDs) accelerate the progression of osteoarthritis by reducing synthesis of vasodilator prostaglandins, thereby diminishing joint perfusion, 105 osteoarthritis patients awaiting hip arthroplasty were treated prospectively with a strong or weak prostaglandin synthesis inhibitor, indomethacin or azapropazone, respectively. Pain and radiological joint space were monitored during the period up to arthroplasty and the condition of the excised femoral head was determined. As judged by radiological and histopathological data, the two treatment groups were at a similar pathophysiological end-point when they came to arthroplasty. In the indomethacin group the affected hips lost joint space more rapidly than did the contralateral hips, a difference not seen in the azapropazone group. The patients receiving azapropazone, who had higher concentrations of synovial vasodilator prostaglandins, took longer than the indomethacin group to reach the arthroplasty end-point. Potent inhibitors of prostaglandin synthesis may be inappropriate in the management of osteoarthritis of the hip.